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Comments of

American Lung Association

Appalachian Mountain Club

Center for Biological Diversity

Clean Air Council

Earthjustice

Environmental Defense Fund

National Parks Conservation Association

Natural Resources Defense Council

Sierra Club

on EPA’s Proposed Revisions to the

National Ambient Air Quality Standards

for Ozone

March 17, 2015

79 FR 75234

Docket ID # EPA-HQ-OAR-2008-0699
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TABLE OF CONTENTS

I. EXECUTIVE SUMMARY................................................................................................... 11

II. LEGAL STANDARD....................................................................................................... 12

A. Overview of Clean Air Act Legal Mandates Governing National Ambient Air Quality 

Standards................................................................................................................................... 12

B. EPA’s Prior Implementation of the Ozone NAAQS ........................................................ 14

C. The Clean Air Act Requires EPA to Set the 2015 Ozone NAAQS at a Level That Protects 

the Public Health of All Americans and That Provides for an Adequate Margin of Safety 

Where There Is Uncertainty...................................................................................................... 15

D. In Setting the Ozone NAAQS EPA Must Err on the Side of Protecting Public Health 

When There Is Scientific Uncertainty....................................................................................... 16

E. EPA Must Also Set the At A Level That Protects Vulnerable Subpopulations ............... 17

F. EPA Cannot Consider the Economic Cost of Meeting the NAAQS ................................ 18

G. EPA Must Give Due Deference to the Advice of CASAC............................................... 18

III. PROCEDURAL BACKGROUND................................................................................... 19

IV. THE EXTENSIVE AND ROBUST BODY OF SCIENTIFIC EVIDENCE 

ESTABLISHES A CLEAR NEED FOR A STANDARD OF 60 PPB IN ORDER TO PROTECT 

THE HEALTH OF ALL AMERICANS WITH AN ADEQUATE MARGIN OF SAFETY...... 20

A. Ozone is Recognized to Cause a Wide Range of Adverse Impacts to Human Health at 

Levels of 60 ppb........................................................................................................................ 20

B. A Number of Subpopulations Are Particularly Susceptible to Exposure to Ozone, 

Including Children .................................................................................................................... 24

1. Scientific Studies Establish Children Are Highly Susceptible to Ozone And Clear 

Risks to Children’s Health Occur at Ozone Levels of 60 ppb............................................... 24

2. Asthmatics Are a Large Subpopulation Highly Sensitive to Ozone, Particularly 

Asthmatic Children................................................................................................................ 29

3. Adult “Responders” Are a Sensitive Population that Must Be Protected Under the 

Revised Standard ................................................................................................................... 34

4. Outdoor Workers, Due to Their Prolonged Exposures to Ambient Air, Are a Sensitive 

Population Requiring Heightened Protection ........................................................................ 34

5. The Elderly Are Also a Large Sensitive Subpopulation At Risk From Ozone ............ 36

6. Recent Evidence Also Suggests New Subpopulations with Heightened Sensitivity to 

Ozone..................................................................................................................................... 36

C. Ozone Can Pose Significant Health Risks for Populations with Pre-Existing Health 

Conditions................................................................................................................................. 37
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1. Obesity is a Pre-Existing Condition Requiring Additional Protection Under the 

Revised NAAQS.................................................................................................................... 37

2. Diabetes is a Pre-Existing Condition Requiring Additional Protection........................ 38

3. COPD is a Pre-Existing Condition Necessitating Additional Protection under the 

Revised Standard ................................................................................................................... 39

4. Heart Disease is a Pre-Existing Condition that Poses Additional Risks When 

Exacerbated by Ozone Exposure........................................................................................... 41

5. Evidence Connects Ozone Exposure to Strokes........................................................... 43

6. Transplant Recipients Are a Sensitive Subpopulation for Ozone Exposure................. 43

7. Cystic Fibrosis is a Pre-Existing Condition Requiring a More Protective Ozone 

Standard................................................................................................................................. 44

8. Due to the Risk of Reproductive and Developmental Effects, Pregnant Women Should 

Be Considered a Sensitive Group.......................................................................................... 45

D. Based on the Demonstrated Impacts to Healthy Individuals at 60 ppb, the Impacts to 

Sensitive Populations at 60 ppb Are Properly Characterized as Adverse ................................ 46

1. Children and Adults with Lung Disease Will Experience Impacts Properly 

Characterized as Adverse Based on Exposures to 60 ppb..................................................... 46

2. Individuals with Pre-existing Pulmonary or Cardiac Disease Will Experience Impacts 

Properly Characterized as Adverse Based on Exposures to 60 ppb ...................................... 47

3. Individuals with Asthma Will Experience Impacts Properly Characterized as Adverse 

Based on Exposures to 60 ppb............................................................................................... 48

4. Lung inflammation in Healthy Adults at 60 ppb is Properly Characterized as Adverse

48

5. Population Level Effects Linked to Ozone Exposures at Levels of 60 ppb are Properly 

Characterized as Adverse. ..................................................................................................... 49

V. COMMENTS ON THE PROPOSAL............................................................................... 49

A. The Current Standard of 75 ppb Does Not Protect the Public Health with an Adequate 

Margin of Safety As Required by the Clean Air Act................................................................ 49

1. Broad Scientific Consensus Supports a More Protective Standard Than 75 ppb ......... 51

a. Since 2008 CASAC Has Consistently Supported Lowering the Standard Below 75 

ppb 51

b. CASAC Concluded That a 70 ppb Standard Provides “Little” Margin of Safety and 

Specifically Cited a Level of 60 ppb as Meeting the Requirements to Protect Public 

Health................................................................................................................................ 53

c. The Children’s Health Protection Advisory Committee Recommends a Standard of 

60 ppb................................................................................................................................ 55
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d. Medical and Public Health Organizations Support a Standard of 60 ppb ................ 56

e. Many Other Countries, and the World Health Organization, Have Concluded That a 

Standard of 75 ppb Is Far Too Weak and that the 65 – 70 ppb Range is Insufficient to 

Protect Public Health. ....................................................................................................... 58

i. World Health Organization..................................................................................... 58

B. EPA’s Proposal of 65-70 Fails to Protect the Public: EPA Must Revise the Primary 

NAAQS to a Level No Higher than 60 ppb.............................................................................. 59

1. The Body of Science Evidence Demonstrates a Compelling Likelihood of Adverse 

Effects to Sensitive Populations at 60 ppb ............................................................................ 59

a. As the ISA Reflects, the Scientific Record is Significantly Stronger in this Review 

than Prior Reviews and Warrants a Standard of 60 ppb ................................................... 60

b. Controlled Studies Demonstrate Lung Function Decrements and Airway 

Inflammation at 60 ppb in Healthy Adults ....................................................................... 62

i. Controlled Human Exposure Studies Demonstrate Lung Function Decrements and 

Airway Inflammation at 60 ppb in Healthy Adults, as well as Pulmonary Inflammation, 

Injury, and Oxidative Stress.......................................................................................... 64

a. Lung Function Decrements and Airway Inflammation................................... 64

b. Pulmonary Inflammation, Injury, and Oxidative Stress.................................. 69

ii. New Models of Controlled Human Exposure Studies Support Data Showing 

Adverse Health Impacts at 60 ppb and Below.............................................................. 70

iii. New Research Confirms Additional Adverse Health Effects in Healthy Adults 

Exposed to Levels of 60 ppb for 6.6 Hours.................................................................. 73

c. Epidemiological Studies Confirm Meaningful Associations Between Mortality, 

Morbidity and Ozone Exposure at Levels Of 70 ppb and Below..................................... 73

i. Findings from Short-Term Epidemiological Studies Compel a Standard of 60 ppb

73

ii. The Current Standard is Not Protective of Public Health ................................... 74

iii. A Standard of 60 ppb is Needed to Protect Public Health .................................. 78

iv. Increased Evidence of Ozone-Caused Mortality in this Review......................... 82

v. Biological Mechanisms....................................................................................... 86

vi. Confidence in the Associations Shown Does Not Decrease at 60 ppb ............... 87

vii. Effects Persist Even After Excluding High Concentration Days above a Certain 

Level 89

viii. EPA Must Base Standards on Concentrations Below the Mean in 

Epidemiological Studies ............................................................................................... 89

ix. Many Additional Epidemiological Studies Show Need for 60 ppb Standard..... 91

x. Studies of Infants, Children, and the Elderly ...................................................... 94
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xi. Two Important New Studies Published Since the Completion of the ISA Provide 

Additional Support for a 60 ppb Standard .................................................................... 99

xii. EPA Analysis Shows that Numerous Studies Have 98th Percentile 8-hour Daily 

Maximum Concentrations Below 70, 65, and 60 ppb ................................................ 101

xiii. Findings from Long-Term Epidemiological Studies Compel a Standard of 60 

ppb 103

xiv. Increased Premature Mortality from Long-Term Exposures ........................ 103

xv. Long-Term Exposure and Survival Rate in People with Pre-existing Conditions

106

xvi. Long-Term Exposures and New Onset Asthma ............................................ 106

xvii. Asthma Hospital Admissions in Children ..................................................... 107

xviii. Asthma Emergency Department Visits and Hospital Admissions................ 108

xix. Long-Term Exposures and Asthma Prevalence ............................................ 109

xx. Low Levels of Ozone over the Long-Term Stunt Lung Function Growth in 

Children....................................................................................................................... 110

xxi. Chronic Ozone Exposure and Lung Damage ................................................ 111

xxii. Pathological Changes to Nasal Passages....................................................... 112

xxiii. Remodeling of the Airways in Toxicology Studies of Primates................... 112

xxiv. A Standard of 60 ppb or Below is Needed to Protect Against Long-Term 

Exposures.................................................................................................................... 112

2. A Standard Above 60 ppb Cannot Be Justified On This Record................................ 117

a. EPA Does Not, and Cannot, Show How Any Level Above 60 ppb Will Protect 

Sensitive Populations with an Adequate Margin of Safety ............................................ 117

b. EPA’s Inconsistent Treatment of Adverse Effects is Arbitrary and Capricious..... 117

c. EPA’s Reliance on Its Exposure Risk Assessment to Reject a Level of 60 ppb Was 

Arbitrary and Capricious, Particularly Because EPA Is Relying On People Not Going 

Outdoors to Conclude That the Level of Air Pollution Outdoors Will Not Harm Them119

i. EPA’s Proposed Range of 65 to 70 ppb Undervalues Exposure Risk for Children 

and Outdoor Workers.................................................................................................. 120

ii. EPA Impermissibly Relies on People Staying Indoors to Avoid Repeated or 

Prolonged Exposure to the Air.................................................................................... 123

iii. The Sufficiency of the NAAQS to Protect Public Health Cannot Depend upon 

Sensitive Populations Remaining Indoors.................................................................. 124

d. EPA’s Risk and Exposure Assessment Has Substantial Limitations that Severely 

Underestimate the Health Impacts of Exposure.............................................................. 126

i. Infants and Small Children Are Excluded ............................................................ 126

ii. A Very Narrow Subset of Health Endpoints are Evaluated .............................. 126

iii. Exposures of Concern are Evaluated for Limited Scenarios............................. 126
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iv. A Risk Function Derived from Study of Healthy Adults Is Inappropriately 

Applied to Children..................................................................................................... 127

v. The Geographic Scope of the Analysis is Limited............................................ 127

vi. EPA Looks at Just Two 3-Year Periods to Estimate Air Quality ..................... 127

vii. The Emission Control Strategies Modeled Are Limited................................... 127

e. Despite These Limitations, the Health Risk and Exposure Assessment and 

Regulatory Impact Analysis Support Setting the Standard at 60 ppb............................. 127

3. EPA Proposes a Form of the NAAQS-- the Fourth Highest 8-hour Maximum Averaged 

Over 3 Years--That Will Fail to Deliver the Public Health Protection that EPA Itself 

Ultimately Concludes is Necessary; Whatever Nominal Level EPA Adopts, the Form Will 

Allow Repeated Exceedances of the Standard Each Season Without Triggering a 

Nonattainment Designation or Any Obligation to Clean up the Air and EPA Must 

Compensate For This By Setting An Accordingly Lower Nominal Level Of The Standard

134

a. Multiple Aspects of the NAAQS Define the Stringency of the Standard............... 135

b. EPA’s Proposed Form and Averaging Time of the NAAQS Requires that the Level 

of the Standard be Lowered to Achieve EPA’s Claimed Level of Health Protection. ... 136

i. An 8-hour Averaging Time is Longer than the Controlled Human Exposure Studies 

Relied upon by EPA; Extrapolating the Results of These Studies to 8 Hours Would 

Produce Larger and More Pervasive Impacts to Test Subjects, Necessitating a Lower 

Level of the NAAQS. ................................................................................................. 136

ii. Because of EPA’s Truncating Conventions, Any Ozone Standard Proposed is, as 

a Practical Matter, a Full Part Per Billion Higher; EPA Must Account for this UnderProtection in Setting the Level of the Standard .......................................................... 137

iii. Because of the Real-World Relationship Between the 3-Year Average of 1st, 2nd

and 4th High 8-hour Daily Monitored Maximum Ozone Concentrations, Use of a 4th

High Form Is Equivalent to Use of a 1st High Form with a Level 7.5 to 8 ppb Higher 

and to a 2nd high Form with a Level 3.5 to 4 ppb higher; EPA Must Account for this 

Under-Protection in Setting the Level of the Standard............................................... 137

c. Under EPA’s Proposed Form of the Standard, a Level of 65 to 70 ppb Would 

Impermissibly Allow, in a Single Ozone Season, Numerous Exposures to Levels Far in 

Excess of Those Acknowledged to be of Concern without Triggering a Nonattainment 

Designation ..................................................................................................................... 143

d. EPA’s Purported Justification for Its Preferred Form Is Arbitrary and Capricious 168

C. The Proposal Fails to Fully and Rationally Explain Reasons for Differing from CASAC’s 

Advice ..................................................................................................................................... 169

1. Primary Standard ........................................................................................................ 169

a. Identification of Adverse Effects............................................................................ 169
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b. Failure to propose a range of the primary standard that includes levels down to 60 

ppb 171

c. EPA’s Inclusion of 70 ppb in the Proposed Range................................................. 175

D. EPA Has Failed To Explain How It Has Accounted For A Margin Of Safety and Has 

Failed To Rationally Explain How The Standards It Has Proposed Incorporate A Margin Of 

Safety That Is Adequate.......................................................................................................... 177

1. EPA Must Set Standards Requisite To Protect The Public Health And Provide For An 

Adequate Margin Of Safety................................................................................................. 177

2. EPA’s Claim that Its Proposal Provides for an Adequate Margin of Safety Is Arbitrary 

and Capricious..................................................................................................................... 177

3. EPA Has Failed to Rationally Explain How the Standards It Has Proposed Incorporate 

an Adequate Margin of Safety............................................................................................. 179

E. Even if EPA Declines to Deviate from Its Proposed Range, EPA Must Set the Standard 

No Higher than 65 ppb, at the Bottom of Its Proposed Range ............................................... 181

F. Public Welfare Secondary National Ambient Air Quality Standard for Ozone ............. 187

1. Introduction................................................................................................................. 187

2. Secondary NAAQS must protect public welfare ........................................................ 188

a. Adverse effects to vegetation and ecosystems........................................................ 189

b. Adverse effects to climate....................................................................................... 189

i. Direct Climate Impacts in the Arctic .................................................................... 190

c. Ecosystem Services................................................................................................. 191

d. Protecting Public Lands.......................................................................................... 191

3. Scientific Consensus Supports a Different Form........................................................ 193

a. Support for a Cumulative Seasonal W126 Standard............................................... 193

b. 8-hr Form Is Not Protective of the Public Welfare................................................. 194

4. The W126 is the right metric ...................................................................................... 199

a. What is the W126 and why is it more relevant to protecting vegetation? .............. 199

b. The CASAC recommendations............................................................................... 200

c. A 12-hr, maximum 3 month W126 form of the standard is conservative .............. 201

5. A Standard of 75 ppb Is Not Protective of the Public Welfare................................... 204

6. The Secondary Standard Must Be Set at a Level No Higher Than 7 ppm-hrs........... 204

a. Visible Foliar Injury................................................................................................ 204

b. Tree biomass; growth and productivity .................................................................. 209

c. Increase protection of carbon storage; benefits to climate change ......................... 210

7. A Range of 13 to 17 ppm-hrs Does Not Assure Requisite Protection........................ 211
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8. EPA’s Proposal Fails to Specify Requisite Levels of Vegetation Protection as Required 

by the Act............................................................................................................................. 213

9. Air Quality Monitoring Requirements........................................................................ 214

a. Changes to length of monitoring seasons ............................................................... 214

b. Need for more monitors in rural and mountain areas............................................. 214

10. SIP Requirements.................................................................................................... 215

a. Attainment Schedule for Secondary Standards Must be Expeditious .................... 215

G. It is Critical For EPA To Set The NAAQS At A Truly Health Protective Level To Allow 

People To Engage In Protective Behavior When The Air Quality Index, Which Is Keyed To 

The NAAQS, Alerts Them That Safe Levels Of Ozone Have Been Exceeded ..................... 215

1. The AQI Must Accurately Inform the Public of Health Hazards From Polluted Air. 216

a. The Primary Purpose of the AQI Is to Facilitate Averting Behavior ..................... 216

b. AQI Values Are Widely Disseminated Through a Robust Infrastructure .............. 217

c. The AQI Is Relied On By Large Numbers of the Population................................. 218

2. Failing to Set the NAAQS At the Health Protective Level of 60 ppb Would Lead to the 

Dissemination of False Information and Rob People of Their Ability to Protect Themselves 

and Their Children From Unsafe Air. ................................................................................. 220

H. Appendix U: EPA’s Proposed Changes to Implementation Rules Would Undermine the 

Health and Welfare-Protectiveness of the Revised Standard and Are Inconsistent with the Act 

and its Regulations.................................................................................................................. 220

1. The Language of the NAAQS Should Not Be Limited to Monitoring Sites; The 

Language Needs to Be Broad Enough to Take into Account the Potential Use of Modeling 

for Evaluating Attainment, Which Should Utilize a Full Receptor Grid Reflecting the Fact 

the NAAQS Are National Ambient Air Quality Standards................................................. 220

2. Data Completeness: EPA Needs to Create a Methodology that Fills in Missing Data, 

Similar to 40 C.F.R. Part 75 of the Acid Rain Program...................................................... 221

3. EPA Should Not Decrease the Number of Monitors Used to Calculate Design Values

222

4. Data Handling: EPA Should Take an Approach that Is Rational, Protective and 

Consistent with the Statute .................................................................................................. 223

5. Changes to Length of Monitoring Seasons................................................................. 224

a. The Length of the Ozone Season Should be a Uniform 12 Months....................... 224

b. Barring Year-Round Monitoring in All Areas, EPA Should Ensure that States Where 

There Is or May Be Winter-Time Ozone Season Problems Including All of the Region 8, 

9 and 10 States, Should Have Year Round Ozone Monitoring ...................................... 225

6. Changes to Monitoring Network ................................................................................ 226
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7. Implementation Issues ................................................................................................ 228

a. Prevention of Significant Deterioration: Significant Emission Rates and Significant 

Impact Levels.................................................................................................................. 228

i. Significant Emission Rates................................................................................... 228

ii. Significant Impact Levels.................................................................................. 230

b. SIP requirements, Schedules and Attainment Dates............................................... 231

c. EPA Has No Authority to “Grandfather” Sources Out of PSD Requirements....... 232

d. Designations............................................................................................................ 237

e. Background Ozone Levels...................................................................................... 238

f. EPA Must Complete Its Reconsideration of the 2008 Ozone NAAQS.................. 239

VI. THE NEW NAAQS IS, AT ITS CORE, ALSO AN ENVIRONMENTAL JUSTICE 

ISSUE: EPA MUST SET A STANDARD THAT IS PROTECTIVE OF MINORITIES AND 

ELIMINATES THE ROLE THAT OZONE PLAYS IN THEIR HEALTH OUTCOMES ...... 240

A. Across the Nation Minorities Disproportionally Live in Higher Levels of Ozone and Thus 

Will Disproportionately Suffer the Impacts of an Insufficient Ozone Standard .................... 241

B. Setting An Ozone Standard That Protects Environmental Justice Communities Requires 

EPA To Consider The Cumulative Impacts Including Synergistic Exposures To Multiple 

Pollutants................................................................................................................................. 253

C. The Environmental Justice Implications of Setting the 2015 NAAQS Are Evident in the 

Asthma Burdens of Minorities, Including in Particular African-Americans.......................... 255

VII. ADDITIONAL CONSIDERATIONS............................................................................ 257

A. Emission Reductions Needed to Improve Air Quality Are Readily Available .............. 257

1. Significant Emission Reductions Are Already Underway and Further Emission 

Reductions Are Readily Achievable.................................................................................... 258

2. Further Reductions in VOC Emissions from the Oil and Gas Sector Are Forthcoming

262

3. There are Significant, Economic Reductions to Be Achieved from Coal Fired 

Electricity Generating Unites in the Electric Power Sector ................................................ 263

4. Additional NOx Reductions from Coal Plants Will Have a Significant Ameliorative 

Effect on Ozone Levels ....................................................................................................... 265

5. Tremendous NOx Reductions--from Coal Fired EGUs as well as from Other Sources--

Can Be Achieved Cost-Effectively And Have Been Judged to Be Economically Reasonable 

Time and Again ................................................................................................................... 270

B. The Benefits of a 60 ppb Ozone Standard Outweigh the Costs...................................... 273

C. The Phenomenon of NOx Scavenging Does Not Counsel a Higher Ozone Standard.... 276

1. Ozone Formation is Complex and Non-Linear........................................................... 276
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2. Ozone Scavenging Is Not A Pollution Control Mechanism – It Is A Pollution-Moving 

Mechanism........................................................................................................................... 278

3. Even If Scavenging Were Relevant, Lowering the Ozone Standard Will Produce 

Health Benefits In All Areas, Including Urban Cores......................................................... 278

a. The Ozone Scavenging Implications of Reduced NOX Emissions Are Extremely 

Limited............................................................................................................................ 278

b. Any Health Risk Increases Resulting From Reduced Ozone Scavenging Are Limited 

at 70 ppb and Offset Entirely at 60 ppb .......................................................................... 279

c. The Effects of Reduced Ozone Scavenging Can Be Mitigated With a Combined 

VOCs/NOx Reduction Strategy...................................................................................... 280

VIII. CONCLUSION............................................................................................................... 280

Appendix of Additional Comments of Members of the Clean Air Scientific Advisory Committee

..................................................................................................................................................... 282
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I. EXECUTIVE SUMMARY

The Clean Air Act requires the U.S. Environmental Protection Agency to set a primary 

National Ambient Air Quality Standard (NAAQS) for ozone pollution at a level that protects 

public health with an adequate margin of safety, and it requires the nation to then achieve 

compliance with that level of air pollution. The Environmental Protection Agency (EPA) has 

appropriately recognized that the existing ozone NAAQS of 75 ppb standard falls far short of 

providing this level of assurance, even for healthy individuals. 

An extensive body of scientific literature unequivocally documents the need for a 60 ppb 

standard. Chamber studies based on exposure of healthy individuals to concentrations of 60 ppb 

for less than 8 hours identified the onset of adverse health effects as defined by the American 

Thoracic Society, the Clean Air Scientific Advisory Council (CASAC), and even the EPA in 

prior iterations of the ozone NAAQS review, including statistically significant lung function 

decrements and airway inflammation. Sensitive populations, including children, asthmatics, the 

elderly, and outdoor workers, exposed to similar concentrations for similar durations are likely to 

experience even more significant impacts. Epidemiological studies bolster the conclusions of the 

controlled human studies and link ozone exposures at levels below 65 ppb to a wide range of 

serious clinical effects including respiratory morbidity and mortality. 

The undersigned groups urge EPA to instead fulfill its unambiguous mandate under the 

Clean Air Act to protect public health by revising the primary ozone NAAQS to the level clearly 

dictated by the science: 60 parts per billion. By EPA’s own assessment, achieving a standard of 

60 ppb, even exclusive of the massive health benefits that would accrue in California, would 

result in as many as 7,900 lives saved, 1.8 million fewer asthma exacerbations for children, and 

1.9 million fewer lost school days each year.1 By contrast, a standard of 65 ppb would achieve 

approximately half of these benefits, and a standard of 70 ppb is projected to save thousands 

fewer lives each year, and avoid only one-sixth of the asthma exacerbations and lost school days 

of a 60 ppb standard. 

Moreover, in adopting a new standard, it is critical that EPA incorporate and provide for 

the fact that the “form” of the standard that EPA proposes to adopt will greatly undermine the 

protective value of the nominal numerical (e.g., 60, 65 or 70 ppb) level of the standard. Under 

the current and proposed form of the standard, areas currently attaining levels of 70 and 65 ppb 

routinely record numerous occurrences of 8-hour daily maximum ozone concentrations of 70 

ppb, 75 ppb, and even 80 ppb and above.2 

 

1 U.S. EPA Regulatory Impact Analysis of the Proposed Revisions to the National Ambient Air 

Quality Standards for Ground-Level Ozone (EPA-452/P-14-006), ES-14-ES-15, Tbl. ES-7 

(2014).

2

Seven years after the 75 ppb standard was established, areas currently meeting the 75 ppb 

NAAQS routinely record numerous exceedances of increments 5 ppb higher (i.e., 75, 80, and 

85); there is no basis to conclude that an analogous distribution of ozone levels would not occur 

under a lower NAAQS. 
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We identify technical flaws in EPA’s exposure assessment that lead to underestimating 

exposures. But more importantly, EPA’s proposed range standard cannot be squared with the 

Clean Air Act because it necessarily requires people—especially sensitive populations such as 

children--to stay indoors to avoid exposures to levels of air quality known to be unhealthful. 

This is all the more problematic because some people do not have an option to limit outdoor 

activity, such as the nearly 9 million workers whose jobs require them to be out of doors all day. 

In addition, a weak ozone standard poses a unique injustice to disadvantaged and 

minority communities. Across the nation, minorities are consistently overrepresented in areas 

with higher ozone levels and that are in nonattainment of ozone NAAQS. Furthermore, across 

the nation the asthma burden of minorities—particularly among blacks—is far higher than that of 

whites. EPA must adopt a 60 ppb standard if it is to protect these communities

Ultimately, the Clean Air Act promises Americans that anyone can go outside whenever 

they want, for as long as they want, and where air quality is attaining the NAAQS it will be safe 

for them to breathe. EPA must adopt a level no higher than 60 ppb if EPA is to fulfill this 

promise. The high end of EPA’s proposal—70 ppb—would be a fundamental betrayal of this 

promise. It would wholly fail to eliminate occurrences of multiple occurrences of levels of 60, 

70, and even 80 ppb. And it is inconsistent with the scientific advice of CASAC, which 

concluded that “[a]t 70 ppb, there is substantial scientific evidence of adverse effects . . . 

including decrease in lung function, increase in respiratory symptoms, and increase in airway 

inflammation.”3 

As for the secondary, welfare-protective, standard, EPA’s proposal to set it identical to the 

primary standard is unlawful and arbitrary. CASAC and the National Park Service have strongly 

endorsed setting a distinct secondary standard to protect vegetation. Thus, to protect vegetation 

and ecosystems and to mitigate anthropogenic climate change, we call for EPA to follow the 

science and set a single-year W126 standard that is no higher than 7 ppm-hrs.

II. LEGAL STANDARD

A. Overview of Clean Air Act Legal Mandates Governing National Ambient Air 

Quality Standards 

The Clean Air Act Amendments of 1970 first introduced the requirement to establish 

enforceable national ambient air quality standards (NAAQS). The amendments were intended to 

be “a drastic remedy to what was perceived as a serious and otherwise uncheckable problem of 

air pollution.” Union Electric Co. v. EPA, 427 U.S. 246, 256 (1976). The 1970 amendments 

“carrie[d] the promise that ambient air in all parts of the country shall have no adverse effects 

upon any American’s health.” 116 Cong. Rec. 42,381 (December 18, 1970).

 

3

Letter from CASAC Chair Dr. H. Christopher Frey to U.S. EPA Administrator Gina McCarthy 

re: Second Draft Policy Assessment for the Review of the Ozone National Ambient Air Quality 

Standards (EPA-CASAC-14-004), ii, June 26, 2014 [hereinafter CASAC Letter 2014a]
13

The NAAQS drive the Clean Air Act’s requirements for controlling emissions of 

conventional air pollutants. Once EPA establishes a NAAQS, states and EPA identify those 

geographic areas that fail to meet the standards. 42 U.S.C. § 7407(d). Each state must prepare 

an “implementation plan” designed to control pollutant emissions in order to reduce the ambient 

concentrations of the pollutant to below the level of the NAAQS and to keep it there.

The Clean Air Act provides a clear process for establishing the NAAQS. The first step in 

establishing a NAAQS involves identifying those pollutants, the “emissions of which, in [EPA’s] 

judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger 

public health or welfare,” and “the presence of which in the ambient air results from numerous or 

diverse mobile or stationary sources.” Id. § 7408(a)(1)(A), (B). Once EPA identifies a pollutant, 

it must select a NAAQS that is based on air quality criteria reflecting “the latest scientific 

knowledge useful in indicating the kind and extent of all identifiable effects on public health or 

welfare which may be expected from the presence of such pollutant in the ambient air.” Id.

§ 7408(a)(2). 

Primary NAAQS must be set at a level “requisite to protect the public health” with “an 

adequate margin of safety.” Id. § 7409(b)(1). To ensure that the NAAQS continue to provide the 

necessary protection, at least every five years, EPA must review and revise as appropriate the 

underlying air quality criteria and the NAAQS themselves to keep pace with scientific 

understanding. Id. § 7409(d)(1). Any primary NAAQS that EPA promulgates under these 

provisions must be adequate to (1) protect public health and (2) provide an adequate margin of 

safety, in order to (3) prevent any known or anticipated health-related effects from polluted air. 

Further, the statute makes clear that there are significant limitations on the discretion granted to 

EPA in selecting a level for the NAAQS. In exercising its judgment, EPA must err on the side of 

protecting public health, and may not consider cost or feasibility in connection with establishing 

the numerical NAAQS or other important elements of the standard (e.g., form of the standard, 

averaging time, etc.). The D.C. Circuit summed up EPA’s mandate succinctly:

Based on these comprehensive [air quality] criteria and taking account of the 

‘preventative’ and ‘precautionary’ nature of the act, the Administrator must then 

decide what margin of safety will protect the public health from the pollutant’s 

adverse effects – not just known adverse effects, but those of scientific 

uncertainty or that ‘research has not yet uncovered.’ Then, and without reference 

to cost or technological feasibility, the Administrator must promulgate national 

standards that limit emissions sufficiently to establish that margin of safety.

American Lung Ass’n v. EPA, 134 F.3d 388, 389 (D.C. Cir. 1998); see also Whitman v. Am. 

Trucking Ass’ns, 531 U.S. 457, 464-71 (2001). Each of these requirements is discussed in more 

detail below.

The Act delegates to the Administrator the responsibility to review and revise NAAQS. 

Thus, neither the Office of Management and Budget (OMB) nor any other agency has authority 

to alter or override the Administrator’s decisions in the review and revision process. Further, 

technical judgments or opinions that appear to come from OMB, and not EPA, are not entitled to 
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judicial deference. See, e.g., Pub. Citizen Health Research Group v. Tyson, 796 F.2d 1479, 1505 

(D.C. Cir. 1986).

B. EPA’s Prior Implementation of the Ozone NAAQS

One of the first pollutants for which EPA adopted NAAQS was ozone, a principal 

component of urban smog, and a severe lung irritant even to healthy adults. See 66 Fed. Reg. 

5002, 5012/3 (Jan. 18, 2001). The first predecessor to the current primary ozone NAAQS was 

promulgated in 1971 at 0.08 ppm, averaged over one hour. 36 Fed. Reg. 8187 (April 30, 1971). 

See Am. Petroleum Inst. v. Costle, 665 F.2d 1176, 1182 (D.C. Cir. 1981) (though the 1971 

standard was nominally addressed to photochemical oxidants, compliance was gauged by 

measuring only ozone). In 1979, EPA relaxed this standard to 0.12 ppm, also averaged over one 

hour. 44 Fed. Reg. 8220 (Feb. 8, 1979).

Subsequently, a growing body of peer-reviewed scientific evidence emerged, 

documenting the inadequacy of the 1979 standard to protect public health with an adequate 

margin of safety. However, despite the Act’s express mandate to review and (as appropriate) 

revise NAAQS at intervals of no greater than five years, 42 U.S.C. § 7409(d)(1), EPA failed to 

consider the new evidence, or to revise the NAAQS to reflect it. 58 Fed. Reg. 13,008, 13,013 

(Mar. 9, 1993) (EPA “missed both the 1985 and 1990 deadlines for completion of [ozone 

NAAQS] review cycles under section 109(d)”). Even after being sued by American Lung 

Association and ordered to complete a review of the NAAQS, EPA issued a final decision that 

still refused to consider the new evidence—and declined to revise the NAAQS. 58 Fed. Reg. at 

13,008, 13,013-14, 13,016. When that decision was challenged in the D.C. Circuit, EPA sought 

and received a voluntary remand to consider the new science. Order of June 27, 1994 in 

American Lung Association v. Browner, D.C. Cir. No. 93-1305.

Finally, many years after the new evidence started to emerge, EPA completed a NAAQS 

review considering that evidence. That review produced the 1997 eight-hour NAAQS, at 0.08 

ppm (equivalent to 0.084 ppm). 62 Fed. Reg. 38,856 (July 18, 1997). After several years of 

litigation, the D.C. Circuit upheld the standard against industry challenge. Am. Trucking Ass’ns 

v. EPA, 283 F.3d 355 (D.C. Cir. 2002); see also Am. Trucking Ass’ns v. EPA, 175 F.3d 1027 

(D.C. Cir. 1999), reh’g granted in part and denied in part, 195 F.3d 4 (D.C. Cir. 1999), aff’d in 

part and rev’d in part sub nom. Whitman v. Am. Trucking Ass’ns, 531 U.S. 457 (2001).

EPA then failed again to timely review and revise the 1997 NAAQS, leading to another 

suit forcing it to carry out its mandatory duty under 42 U.S.C. § 7409(d). Am. Lung Ass’n v. 

Whitman, No. 03-CV-778 (D.D.C.). In the review process, the Clean Air Scientific Advisory 

Committee (CASAC), which is charged with reviewing the air quality criteria and NAAQS and 

making scientific recommendations on them, unanimously found that the primary NAAQS 

should be revised to a level between 0.060 and 0.070 ppm. In 2008, EPA disagreed with 

CASAC and set the primary standard at 0.075 ppm. 73 Fed. Reg. 16,436 (Mar. 27, 2008).

Soon thereafter, EPA itself raised concerns about whether its 2008 standards complied 

with the Act and began a reconsideration of the NAAQS. In early 2010, based solely on the 

information already before it, EPA proposed to strengthen the primary NAAQS to somewhere 
15

within the CASAC-recommended range of 0.060-0.070 ppm. 75 Fed. Reg. 2938 (Jan. 19, 2010). 

The proposal stated that the Administrator “judge[d] that a standard level of 0.075 ppm is not 

sufficient to provide [health] protection with an adequate margin of safety.” Id. at 2996/2. EPA 

ultimately declined to finalize its proposed reconsideration, instead assuring the D.C. Circuit that 

it would address the reconsideration when it completed its next review and revision of the ozone 

NAAQS. See Mississippi v. EPA, 744 F.3d 1334, 1341-42 (D.C. Cir. 2013). Ultimately, the D.C. 

Circuit upheld the 2008 standard. Id. at 1342.

The 2008 standard was due for review and revision in 2013. Because EPA missed the 

deadline, American Lung Association, Sierra Club, and others again sued EPA and obtained an 

order requiring EPA to complete this review by October 1, 2015. Order, Sierra Club v. EPA, No. 

13-CV-2809 (N.D. Cal. Apr. 30, 2014).

C. The Clean Air Act Requires EPA to Set the 2015 Ozone NAAQS at a Level 

That Protects the Public Health of All Americans and That Provides for an 

Adequate Margin of Safety Where There Is Uncertainty

In setting or revising a primary NAAQS, section 109 of the Clean Air Act requires that 

EPA assure the protection of public health with an adequate margin of safety. As noted above, 

this mandate “carries the promise that ambient air in all parts of the country shall have no 

adverse effects upon any American’s health.” 116 Cong. Rec. 42,381 (Dec. 18, 1970) (remarks 

of Senator Muskie, floor manager of the conference agreement). Thus:

Standards must be based on a judgment of a safe air quality level and not on an 

estimate of how many persons will intersect given concentration levels. EPA 

interprets the Clean Air Act as providing citizens the opportunity to pursue their 

normal activities in a healthy environment.

44 Fed. Reg. at 8210. Thus, as EPA has acknowledged, it cannot deny Americans protection 

from the effects of air pollution by claiming that the people experiencing those effects are 

insufficiently numerous, or that levels that are likely to cause adverse health effects occur only in 

areas that are infrequently visited.4

Likewise, in implementing the mandates in section 109(b) and setting the NAAQS, EPA 

cannot deny protection against adverse health and welfare effects merely because those effects 

are confined to subgroups of the population or to persons especially sensitive to air pollution. 

 

4

See also 116 Cong. Rec. 32,901 (Sept. 21, 1970) (remarks of Senator Muskie) (“This bill states that all Americans 

in all parts of the Nation should have clean air to breathe, air that will have no adverse effects on their health.”); id.

at 33,114 (Sept. 22, 1970) (remarks of Senator Nelson) (“This bill before us is a firm congressional statement that all 

Americans in all parts of the Nation should have clean air to breathe, air which does not attack their health.”); id. at 

33,116 (remarks of Senator Cooper) (“The committee modified the President’s proposal somewhat so that the 

national ambient air quality standard for any pollution agent represents the level of air quality necessary to protect 

the health of persons.”); id. at 42,392 (Dec. 18, 1970) (remarks of Senator Randolph) (“we have to insure the 

protection of the health of the citizens of this Nation, and we have to protect against environmental insults -- for 

when the health of the Nation is endangered, so is our welfare, and so is our economic prosperity”); id. at 42,523 

(remarks of Congressman Vanik) (“Human health and comfort has been placed in the priority in which it belongs --

first place.”).
16

See, e.g., Nat’l Envtl. Dev’t Ass’n’s Clean Air Project v. EPA, 686 F.3d 803, 810 (D.C. Cir. 

2012). It is inherent in NAAQS-setting that adverse effects are experienced by less than the 

entire population, and that we do not know in advance precisely which individuals will 

experience a given effect. As a result, opponents of protective NAAQS sometimes argue that 

NAAQS-setting involves evaluating “risk” and setting a level of risk that is “acceptable.” But 

where—as here—peer-reviewed science shows that adverse effects stem from a given pollutant 

concentration, EPA must set NAAQS that protect against that given pollution concentration and 

the health effects that result from that level of concentration of pollution, while providing an 

adequate margin of safety. It cannot, under the guise of risk management, set NAAQS that allow 

such effects to persist. Indeed, given the scientific evidence documenting the occurrence of 

adverse effects year after year in numerous individuals at levels allowed by the current NAAQS, 

risks are by definition “significant” enough to require protection under the Act’s protective and 

precautionary approach. See H. Rep. No. 95-294, at 43-51 (1977); Ethyl Corp. v. EPA, 541 F.2d 

1 (D.C. Cir. 1976) (en banc). That is all the more true where the effects involved include highly 

serious ones like death and hospitalization. See Ethyl Corp., 541 F.2d at 18 (“the public health 

may properly be found endangered ... by a lesser risk of a greater harm”).

D. In Setting the Ozone NAAQS EPA Must Err on the Side of Protecting Public 

Health When There Is Scientific Uncertainty

The D.C. Circuit has characterized the NAAQS as “preventative in nature.” E.g., Ethyl 

Corp., 541 F.2d at 15; see also H. Rep. No. 95-294, at 49-51 (explaining amendments designed 

inter alia “[t]o emphasize the preventive or precautionary nature of the act, i.e., to assure that 

regulatory action can effectively prevent harm before it occurs”). The Act’s mandate requires 

that in considering uncertainty EPA “must err on the side of caution” in terms of protecting 

human health and welfare: “The Act requires EPA to promulgate protective primary NAAQS 

even where ... the pollutant’s risks cannot be quantified or ‘precisely identified as to nature or 

degree.’” E.g., Am. Trucking Ass’ns, 283 F.3d at 369, 378.

Thus, in keeping with the precautionary and preventative nature of the NAAQS, EPA 

must set a new ozone standard that protects against potential adverse health effects—not just 

those impacts that have been well established by science. See Am. Trucking Ass’ns, 283 F.3d at 

369 (citing 1997 Ozone NAAQS, 62 Fed. Reg. 38,857 (section 109(b)(1)’s “margin of safety 

requirement was intended to address uncertainties associated with inconclusive scientific and 

technical information ... as well as to provide a reasonable degree of protection against hazards 

that research has not yet identified”)); see also API v. EPA, 684 F.3d 1342, 1352 (D.C. Cir. 

2012).

In the seminal case on the NAAQS, the D.C. Circuit found that Congress “specifically 

directed the Administrator to allow an adequate margin of safety to protect against effects which 

have not yet been uncovered by research and effects whose medical significance is a matter of 

disagreement.” Lead Indus. Ass’n v. EPA, 647 F.2d 1130, 1154 (D.C. Cir. 1980). Limited data 

are not an excuse for failing to establish the level at which there is an absence of adverse effect. 

To the contrary, “Congress’ directive to the Administrator to allow an ‘adequate margin of

safety’ alone plainly refutes any suggestion that the Administrator is only authorized to set 

primary air quality standards which are designed to protect against health effects that are known 
17

to be clearly harmful.” Id. at 1154-55.

In another case dealing with this same “margin of safety” requirement, the D.C. Circuit 

rejected industry’s argument that EPA was required to document “proof of actual harm” as a 

prerequisite to regulation, instead upholding EPA’s conclusion that the Act contemplates 

regulation where there is “a significant risk of harm.” Ethyl Corp., 541 F.2d at 12-13. Noting the 

newness of many human alterations of the environment, the court found:

Sometimes, of course, relatively certain proof of danger or harm from such 

modifications can be readily found. But, more commonly, ‘reasonable medical 

concerns’ and theory long precede certainty. Yet the statute — and common sense 

— demand regulatory action to prevent harm, even if the regulator is less than 

certain that harm is otherwise inevitable.

Id. at 25; accord Industrial Union Dept. v. Am. Petroleum Inst., 448 U.S. 607, 655-56 (1980) 

(agency need not support finding of significant risk “with anything approaching scientific 

certainty,” but rather must have “some leeway where its findings must be made on the frontiers 

of scientific knowledge,” and “is free to use conservative assumptions in interpreting the data,” 

“risking error on the side of overprotection rather than underprotection”). Rather, as discussed 

above, EPA must take a protective and precautionary approach that errs on the side of caution in 

interpreting uncertainty.

E. EPA Must Also Set the At A Level That Protects Vulnerable Subpopulations

Importantly, the NAAQS must be set at levels that are not only adequate to protect the 

average member of the population, but also guard against adverse effects in vulnerable 

subpopulations, such as children, the elderly, and people with heart and lung disease. In fact, the 

D.C. Circuit has repeatedly found that if a certain level of a pollutant “adversely affects the 

health of these sensitive individuals, EPA must strengthen the entire national standard.” 

American Lung Ass’n, 134 F.3d at 390 (citations omitted); see also Coal. of Battery Recyclers 

Ass’n v. EPA, 604 F.3d 613, 618 (D.C. Cir. 2010); Am. Farm Bureau Fed’n v. EPA, 559 F.3d 

512, 524 (D.C. Cir. 2009). EPA must also build into the NAAQS an adequate margin of safety 

for these sensitive subpopulations. See Am. Farm Bureau Fed’n, 559 F.3d at 526.

The drafters of the 1970 Clean Air Act Amendments made clear that the millions of 

Americans subject to respiratory ailments are entitled to the protection of the NAAQS: “Included 

among those persons whose health should be protected by the ambient standard are particularly 

sensitive citizens such as bronchial asthmatics and emphysematics who in the normal course of 

daily activity are exposed to the ambient environment.” S. Rep. No. 91-1196, at 10 (1970). As 

the D.C. Circuit has explained:

In its effort to reduce air pollution, Congress defined public health broadly. 

NAAQS must protect not only average healthy individuals, but also “sensitive 

citizens” – children, for example, or people with asthma, emphysema, or other 

conditions rendering them particularly vulnerable to air pollution.
18

American Lung Ass’n, 134 F.3d at 390 (citations omitted); Nat’l Envtl. Devel. Ass’n’s Clean Air 

Project, 684 F.3d at 810. Stated another way, NAAQS must “be set at a level at which there is 

‘an absence of adverse effect’ on these sensitive individuals.” Lead Indus. Ass’n, 647 F.2d at 

1153.

By the best estimates, over 85 million Americans have cardiovascular disease;512.7 

million have been diagnosed with Chronic Obstructive Pulmonary Disease (COPD), which 

includes both emphysema and chronic bronchitis;6and 25.9 million Americans, including 7.1 

million children, have chronic asthma.7 Considering that these disease categories alone 

encompass one-third of the population of the United States, the public health implications are 

enormous. Children and the elderly are additional populations at increased risk from ozone air 

pollution, according to the Integrated Science Assessment (ISA).8There are 74 million children 

under 18 and 40 million adults over 65 in the United States. Proposed Rule at 75,269/2. 

Socioeconomic status—living in poverty—may also be risk factor, per the ISA. According to the 

Census Bureau, 45.3 million people live in poverty.9

F. EPA Cannot Consider the Economic Cost of Meeting the NAAQS

In setting or revising a NAAQS, EPA cannot consider the economic impact of the 

standard—only the impact on public health. Lower courts had long held that costs could not be 

considered in setting NAAQS, and in 2001, the Supreme Court affirmed this position. Justice 

Scalia, writing for a unanimous Court, found that the plain language of the statute makes clear 

that economic costs cannot be considered: “Were it not for the hundreds of pages of briefing 

respondents have submitted on the issue, one would have thought it fairly clear that this text does 

not permit the EPA to consider costs in setting the standards.” Whitman, 531 U.S. at 465.

G. EPA Must Give Due Deference to the Advice of CASAC

The Act expressly requires EPA, in developing standards, to consider the advice of the 

statutorily created Clean Air Scientific Advisory Committee (CASAC) and rationally explain 

any important departure from CASAC’s recommendations. 42 U.S.C. §§ 7409(d)(2)(B), 

7607(d)(3). When CASAC makes a scientific finding, it is not enough for EPA merely to 

“disagree” with CASAC’s findings on policy grounds: “to the extent that CASAC has exercised 

scientific judgment, EPA must respond in kind.” Mississippi, 744 F.3d at 1358. Nor can EPA 

rotely invoke “uncertainty” to justify disagreeing with CASAC’s scientific judgment. Id. at 1357. 

 

5 D. Mozaffarian et al., on behalf of the American Heart Association Statistics Committee and Stroke Statistics

Subcommittee . Heart disease and stroke statistics—2015 update: a report from the American Heart Association, 

Circulation, 131: e29-e322, e156 (2015).

6 CDC, National Center for Health Statistics. National Health Interview Survey Raw Data (2011). Calculations by 

the American Lung Association Research and Health Education Division using SPSS and SUDAAN software.

7 CDC. Behavioral Risk Factor Surveillance System (2011); accord 79 Fed. Reg. 75,269/2 (Dec.17, 2014 

)[hereinafter Proposed Rule] (“more than 25 million people” have asthma, and, specifically, 9.5% of the 74 million 

children in the United States—more than 7 million—have asthma). 

8 U.S. EPA, Integrated Science Assessment for Ozone and Related Photochemical Oxidants (EPA/600/R-10/076F) 

(2013).

9 C. DeNavas-Walt & D.B. Bernadette, U.S. Census Bureau, Current Population Reports, Income and Poverty in the 

United States: 2013 (P60-249) 12 (2014), available at 

http://www.census.gov/content/dam/Census/library/publications/2014/demo/p60-249.pdf.
19

Instead, “EPA must explain why the evidence on which CASAC relied cannot support the degree 

of confidence CASAC placed in it. This is especially true given the added layer of stringency 

imposed by EPA’s obligations under section 307(d)(6).” Id.

Even if CASAC makes a policy, rather than scientific, recommendation that EPA departs 

from, EPA must explain its reasoning for not accepting the recommendations of CASAC. Am. 

Farm Bureau Fed’n, 559 F.3d at 521. Even if the Act did not so require, settled principles of 

administrative law would require EPA to reconcile any disparity between its standards and those 

recommended by CASAC. Motor Vehicle Mfrs. Ass’n v. State Farm Mut. Auto. Ins. Co., 463 

U.S. 29, 43 (1983).

III. PROCEDURAL BACKGROUND

In 2009, after consultation with CASAC and the public, EPA revised the procedure for 

the NAAQS review process. The new, clearly defined process was used for the first time in this 

review cycle for the ozone NAAQS. The review was conducted over a period of five years, with 

public participation and peer review by CASAC at every step of the process. The chronology 

below demonstrates that the NAAQS review process undertaken for ozone was extraordinarily 

thorough, with many checks and balances. 

One of the procedural changes incorporated into the revised review process is the 

convening of a scientific workshop at the beginning of the review to help frame the most 

significant scientific issues. More specifically, in October 2008, EPA issued a public call for 

new information regarding ozone. Later that month, EPA convened a workshop on the ozone 

NAAQS, inviting experts in the field to participate panel presentations on new scientific 

developments relevant to the review of the ozone NAAQS. 

Based on the workshop discussions, EPA developed a draft Integrated Review Plan 

(IRP), in February 2009, laying out a plan and a schedule for the ozone NAAQS review, which 

was reviewed by CASAC and the public. EPA then developed an Integrated Science 

Assessment (ISA) as the next step in the review process. This entailed a thorough literature 

search and a rigorous assessment of the scientific literature. Prior to the publication of the first 

draft of the document, in August 2010, EPA convened a workshop with invited experts and the 

public to review the preliminary draft chapters. 

EPA then published a first draft of the ISA in February 2011, and invited public 

comments on the document. CASAC likewise convened a two-day meeting in May 2011 to hear 

comments from the public and to review the draft document. The Committee developed 

extensive written comments to the Agency, recommending revisions to the draft document. EPA 

released a second draft ISA in September 2011. As usual, the agency received written and oral 

comments on the document from the public, and a detailed review by CASAC. During its indepth peer review, CASAC recommended many changes in the document which necessitated 

development of a third draft ISA, which was issued in June 2012. Although not part of the 

original protocol, this additional step demonstrates that this was a fully open, public process that 

recognized and addressed the concerns of both independent scientists and public commenters. 

The final ISA of 1,250 pages was published in February 2013. More than two thousand studies 
20

are cited in the bibliography for the ISA, including one thousand studies new to this review. 

While EPA was in the process of drafting the ISA, it was also undertaking the Health 

Risk and Exposure Assessment (HREA) and Welfare Risk and Exposure Assessment (WREA). 

More specifically, after publication of the first draft ISA, in April 2011, EPA released a detailed 

plan for the development of the HREA and WREA. This plan was also subject to public 

comments and peer review by CASAC. In August 2012, EPA then released first drafts of the 

HREA, WREA, and the Policy Assessment (PA). These documents underwent extensive review 

by CASAC and the public. They were followed by a second draft HREA, WREA, and PA in 

January 2014, which were also subject to public comment and review by CASAC. The final 

HREA, WREA, and PA were finalized in August and published in September 2014. 

All told, CASAC met 15 days through public meetings and public teleconferences to 

review draft versions of the various documents, including the IRP, the ISA, the HREA, the 

WREA, and the PA. The CASAC panel submitted hundreds of pages of comments, individually, 

and as a whole. 

The review of the ozone NAAQS led to recommendations by CASAC and EPA staff 

scientists for revisions to the standards. For the primary, public health standard, the EPA 

scientific staff recommended a range of 60 to 70 ppb, while CASAC endorsed a range of 60 to 

somewhat below 70 ppb. Given the conclusions of CASAC, the Policy Assessment and the 

evidence before EPA, there is no reasoned basis for EPA’s failure to specify 60 ppb as the low 

end of its proposed range. Indeed, as discussed below, all of the evidence indicates that the 

standard must be set at a level at least as protective as 60 ppb. 

IV. THE EXTENSIVE AND ROBUST BODY OF SCIENTIFIC EVIDENCE 

ESTABLISHES A CLEAR NEED FOR A STANDARD OF 60 PPB IN ORDER 

TO PROTECT THE HEALTH OF ALL AMERICANS WITH AN ADEQUATE 

MARGIN OF SAFETY

A. Ozone is Recognized to Cause a Wide Range of Adverse Impacts to Human 

Health at Levels of 60 ppb

Exposure to ozone is connected to a wide range of significant human health impacts. 

Serious physiological effects result from both single incidents of exposure at high concentrations 

and from repeat exposures over time, even for healthy individuals and at relatively low 

concentrations. Adverse health effects including respiratory and cardiovascular morbidity, 

premature mortality, and central nervous system and developmental impacts have been 

demonstrated through controlled human exposure, epidemiologic, and toxicological studies.10

While the impacts of acute ozone exposure are better understood, there is a growing body of 

scientific evidence showing long-lasting adverse impacts of chronic ozone exposure, which may 

be more severe and less reversible. 

Exposure to ozone, both in the short-term (acute) and long-term (chronic), is known to 

 

10 See generally U.S. EPA (2013). Integrated Science Assessment for Ozone and Related Photochemical Oxidants 

(EPA/600/R-10/076F ) [hereinafter ISA]. 
21

cause or exacerbate respiratory impacts such as breathing discomfort (e.g., coughing, wheezing, 

shortness of breath, pain upon inspiration), decreasing lung function and capacity, and lung

inflammation and injury. Research on the relationship between ozone exposure and respiratory 

effects is well-documented and in fact, EPA’s ISA made a conclusive determination that shortterm exposure to ozone is responsible for adverse respiratory effects.

11 Studies have consistently 

demonstrated that exposure to relatively low concentrations of ozone is associated with lung 

function decrements, increases in respiratory symptoms, pulmonary inflammation in children 

with asthma, increases in respiratory-related hospital admissions and emergency department 

visits, and respiratory mortality. In addition, the ISA concludes there is a “likely causal” 

relationship between long-term exposure and adverse respiratory effects such as pulmonary 

inflammation and injury, new onset asthma, and respiratory mortality, and EPA finds an “overall 

strong body of evidence of adverse health effects.”12

Ozone exposure is shown to result in respiratory tract inflammation and epithelial 

permeability. Inflammation can be considered evidence that injury has occurred.13 Acute ozone 

exposure initiates an inflammatory response throughout the respiratory tract that has been 

observed to persist for at least 18-24 hours following the exposure.14 This inflammation can 

evolve into a chronic inflammatory state and repeat episodes can alter the structure and function 

of tissues, leading to a “scarring” or “stiffening” of the lung tissue, such as pulmonary fibrosis. 

Lung tissue (epithelium or lining) may thus experience damage from chronic exposure to even 

relatively low levels of ozone. Inflammation can also alter the body’s host defense response to 

inhaled microorganisms, particularly in sensitive groups, and responses to agents like allergens 

or toxins. Studies suggest that acute ozone exposure might impair lung host defense capability, 

resulting in a predisposition to bacterial infections in the lower respiratory tract.15

Short-term exposure to ozone results in bronchoconstriction—the tightening or narrowing 

of airways in the lungs—and in airway obstruction, causing coughing, wheezing, and shortness 

of breath. Ozone exposure has been shown to cause an increase in airway hyperresponsiveness, 

a condition in which the airways undergo enhanced bronchoconstriction.16 Ozone-induced 

airway hyperresponsiveness results in a predisposition for bronchial narrowing upon inhalation 

of a variety of ambient stimuli. Symptoms have been demonstrated in both asthmatics and 

healthy individuals, although asthmatics are at higher risk due to already having greater airway 

inflammation and bronchial reactivity.

Ozone exposure harms lung function. As controlled human exposure studies and panel 

 

11 Id. sec. 6.2. 

12 Id. at 1-5; U.S. EPA (2014). Policy Assessment for the Review of the Ozone National Ambient Air Quality

Standards (EPA-452/R-14-006) 3-40 [hereinafter Policy Assessment].

13 ISA at 6-76.

14

 See ISA sec. 6.2.3; A. Torres et al. (1997). Airway inflammation in smokers and nonsmokers with varying 

responsiveness to ozone, Am. J. Respir. Crit. Care Med., 156(3): 728-736; I.S. Mudway & F.J. Kelly (2004). An 

investigation of inhaled ozone dose and the magnitude of airway inflammation in healthy adults, Am. J. Respir. Crit. 

Care Med., 169(10): 1089-1095.

15 See ISA sec. 6.2.5.5.

16

 See ISA sec. 6.2.2; see also D.H. Horstman et al. (1990). Ozone concentration and pulmonary response 

relationships for 6.6-hour exposures with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm, Am. J. Respir. 

Crit. Care Med., 142(5): 1158-1163; R. Jörres, D. Nowak, & H. Magnussen (1996).The effect of ozone exposure on 

allergen responsiveness in subjects with asthma or rhinitis, Am. J. Respir. Crit. Care Med., 153(1); 56-64.
22

studies demonstrate, respiratory responses to acute ozone exposure include decreased breathing 

capacity, rapid and shallow breathing, and painful inhalation. These changes are reported 

following exposures to relatively low ambient ozone concentrations, particularly in sensitive 

groups such as children and outdoor workers. Studies examining lung function decrements 

following outdoor activity show robust associations with ozone concentrations at 60 ppb and 

below17 and even down to 40 ppb.18 Early lung function deficits in children may lead to lower 

maximum lung function later in life, as well as to increased risk of respiratory disease,

cardiovascular morbidity, and mortality.19 For adults, chronic ozone exposure is tied to lasting 

declines in lung function and other respiratory effects.20

Not only is ozone exposure linked to the exacerbation of existing asthma, but also to new 

cases of the disease. Individuals with asthma are at greater risk for experiencing ozone-related 

health effects, especially children. Children living in areas with high ambient ozone 

concentrations were found in one study to be more likely to either have asthma or to experience 

asthma attacks compared to children living in areas with lower concentrations.21 The relationship 

between asthma and ozone exposure is supported by evidence of increases in respiratory asthma 

medication use and asthma-related hospital and emergency room visits following exposure.

Evidence also points to long-term exposure causing new-onset asthma. For adults, studies show 

increased risk for developing asthma with each 10 ppb increase in annual mean ozone or 8-hour 

average.

22 Not surprisingly, ozone is also connected to new onset asthma in children.23

 

An expanding body of research reveals causal relationships between ozone exposure and 

cardiovascular health.24 Controlled human exposure studies document negative cardiovascular 

effects in response to short-term ozone exposure, including changes in heart rate variability and 

blood markers of systemic inflammation and oxidative stress, further supporting effects observed 

 

17 B. Brunekreef, et al. (1994). Respiratory effects of low-level photochemical air pollution in amateur cyclists, Am. 

J. of Resp. and Crit. Care Med., 150(4): 962-966; D.M. Spektor et al. (1988). Effects of ambient ozone on 

respiratory function in active, normal children, Am. Rev. of Resp. Disease, 137(2): 313-320; M.H. Gielen, S.C. van 

der Zee, J.H. van Wijnen, C.J. van Stehen, & B. Brunekreef (1997). Acute effects of summer air pollution on 

respiratory health of asthmatic children, Am. J. Respir. Crit. Care Med., 155(6): 2105-2108.

18 M. Brauer, J. Blair, & S. Vedal (1996). Effect of ambient ozone exposure on lung function in farm workers, Am. 

J. of Resp. and Crit. Care Med., 154(4): 981-987. 

19 R. Rojas-Martinez, et al. (2007). Lung Function Growth in Children with Long-Term Exposure to Air Pollutants 

in Mexico City, Am. J. Respir. Crit. Care Med., 176(4): 377-384. 

20 A. Galizia & P.L. Kinney, Long-Term Residence in Areas of High Ozone: Associations with Respiratory Health 

in a Nationwide Sample of Nonsmoking Young Adults (1999). Environ. Health Perspect., 107(8): 675-679; N. 

Künzli et al. (1997). Association between Lifetime Ambient Ozone Exposure and Pulmonary Function in College 

Freshmen: Results of a Pilot Study, Environ Res., 72(1), 8-23; I.B. Tager, et al. (2005). Chronic Exposure to 

Ambient Ozone and Lung Function in Young Adults, Epidemiology, 16(6): 751-759. 

21 L.J. Akinbami, C.D. Lynch, J.D. Parker, & T.J. Woodruff (2010). The association between childhood asthma 

prevalence and monitored air pollutants in metropolitan areas, United States, 2001-2004, Environ Res., 110(3): 294-

301.

22

 W.F. McDonnell, D.E. Abbey, N. Nishino, & M.D. Lebowitz (1999). Long-term ambient ozone concentration 

and the incidence of asthma in nonsmoking adults: the AHSMOG study, Environ. Res., 80(2): 110-121; J. Greer, 

D.E. Abbey, & R.J. Burchette (1993). Asthma related to occupational and ambient air pollutants in nonsmokers, J. 

Occup. Environ. Med., 35(9): 909-915.

23 See e.g., R. McConnell et al. (2002). Asthma in exercising children exposed to ozone: A cohort study, Lancet, 

359(9304): 386-391. 

24 See ISA sec. 6.3 and 7.3.
23

in toxicological studies.25 Ozone exposure is shown to be associated with increased risks of heart 

attacks, coronary atherosclerosis, stroke, and heart disease, even at very low concentrations; one 

study showed positive correlations between these impacts and mean concentrations of 25 ppb 

and maximum concentrations of only 40.2 ppb.

26 More new studies link ozone exposure to 

increased risk for heart attacks27 and stroke incidents.28 Chronic ozone exposure may put 

children at risk for cardiovascular disease later in life and young adults growing up in areas with 

higher ozone concentrations have shown a tendency towards early atherosclerotic (hardening of 

the arteries).29

Short- and long-term ozone exposure has been linked to premature mortality.30

Epidemiological studies show a strong relationship between short-term ozone exposure and 

premature mortality. The ISA describes numerous studies across the U.S., Canada, and Europe

that link ambient ozone concentrations with respiratory mortality, finding that on average it 

occurs at mean 8-hour maximum concentrations of less than 63 ppb.

31 In one key study of 98 

U.S. cities, mean concentrations of only 26.8 ppb were associated with mortality and a 10 ppb 

increase in the prior week’s ozone level increased mortality by 0.52 percent.32 Higher risks were 

also associated with factors such as race and socioeconomic status. Another large U.S. cohort 

study showed a significant increase in the risk of death from respiratory causes in association 

with long-term exposure to ozone.33 Some studies have shown relationships between long-term 

ozone exposures and cardiopulmonary mortality as well.34

Other health impacts linked to ozone exposure are related to newborns and developing 

 

25 R.B. Devlin et al. (2012). Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects, 

Circulation, 126(1):104-111; H. Gong et al. (1998). Cardiovascular effects of ozone exposure in human volunteers, 

Am. J. Respir. Crit. Care Med., 158(2): 538-546; L. Liu (1999). A comparison of biomarkers of ozone exposure in 

human plasma, nasal lavage, and sputum, Inhalation Toxicology, 11(8), 657-674.

26 P. Koken et al. (2003). Temperature, air pollution, and hospitalization for cardiovascular diseases among elderly 

people in Denver, Environ Health Perspec. 111(10): 1312-1317.

27 K.B. Ensor, L.H. Raun, & D. Persse (2013). A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and 

Air Pollution, Circulation, 127(11):1192-1199; S. von Klot et al. (2005). Ambient Air Pollution is Associated with 

Increased Risk of Hospital Cardiac Readmissions of Myocardial Infarction Survivors in Five European Cities, 

Circulation , 112(5): 3073-3079; J. Ruidavets et al. (2005). Ozone Air Pollution is Associated with Acute 

Myocardial Infarction, Circulation, 111(5): 563-569. 

28 J.B. Henrotin, J.P. Besancenot, Y. Bejot, & M. Giroud (2007). Short-term effects of ozone air pollution on 

ischaemic stroke occurrence: a case-crossover analysis form a 10-year population-based study in Dijon, France, 

Occup. Environ. Med., 64(7):4439-445; D.Q. Rich et al. (2006). Increased Risk of Paroxysmal Atrial Fibrillation 

Episodes Associated with Acute Increases in Ambient Air Pollution, Environ. Health Perspec., 114(1):120-123. 

29 C.V. Breton et al. (2012). Childhood air pollutant exposure and carotid artery intima-media thickness in young 

adults, Circulation, 126(13): 1614 –1620; S.D. Adar (2012). Childhood exposures to ozone: the fast track to 

cardiovascular disease?, Circulation, 126(13):1570-1572.

30 The ISA concludes that there is a “likely causal” relationship between short-term ozone increases and total 

mortality. Chronic ozone exposure was “suggestive of a causal relationship” with premature mortality. 

31 ISA at 2-22.

32 M.L. Bell & F. Dominici (2008). Effect modification by community characteristics on the short-term effects of 

ozone exposure and mortality in 98 US communities, Am. J. of Epidem., 167(8): 986-997. 

33 M. Jerrett et al. (2009). Long-term ozone exposure and mortality, New Eng. J. of Med., 360(11): 1085-1095.

34 K.R. Smith et al. (2009). Public health benefits of strategies to reduce greenhouse-gas emissions: Health 

implications of short-lived greenhouse pollutants, Lancet, 374(9707): 2091-2103; A. Zanobetti & J. Schwartz 

(2011). Ozone and Survival in Four Cohorts with Potentially Predisposing Diseases, Am. J. Respir. Crit. Care Med., 

184: 836-841.
24

fetuses.

35 Although research on these effects is less developed, existing evidence presents serious 

public health concerns and additional support for enacting a lower primary standard that protects 

public health and provides a precautionary margin of safety. Prenatal ozone exposure has been 

linked to reduced birth weight, premature delivery, and birth defects. Studies have observed 

associations between lower birth weight and intrauterine growth retardation and prenatal ozone 

exposure.36 Prenatal exposure to elevated ozone concentrations has also been associated with 

premature birth37 and with birth defects in some studies.38 The effects of pre-natal ozone 

exposure may persist after birth. One study of eight U.S. cities with mean 8-hour concentrations 

of only 48 ppb showed that children born prematurely or with low birth weight are more 

susceptible to ozone-related health impacts.39 Another recent study demonstrated that prenatal 

ozone exposure leads to increased need for health care, with the costs of health care in the first 

days after birth increasing by $964 per unit (ppm).40

Finally, new research is suggestive of a relationship between ozone exposure and effects 

on the central nervous system. 41 Studies show that acute ozone exposure may be linked to 

alterations in neurotransmitters, motor activity, short- and long-term memory, sleep patterns, and 

signs of neurodegeneration.

B. A Number of Subpopulations Are Particularly Susceptible to Exposure to 

Ozone, Including Children 

As noted above, people with asthma and other respiratory or pulmonary health conditions 

are particularly susceptible to exposure to ozone and can have more severe reactions to lower 

levels of ozone than the general population. However, other especially sensitive subpopulations 

exist as well. These are discussed separately below.

1. Scientific Studies Establish Children Are Highly Susceptible to Ozone 

And Clear Risks to Children’s Health Occur at Ozone Levels of 60 

ppb 

 

35 Finding greater evidence than in the last review, the ISA concludes that research is “suggestive of a causal 

relationship” between long-term exposures to ozone and reproductive and developmental effects. 

36 M.T. Salam et al. (2005). Birth Outcomes and Prenatal Exposure to Ozone, Carbon Monoxide, and Particulate 

Matter: Results from the Children’s Health Study, Environ. Health Perspec. 113(11): 1638-1644; R. MorelloFrosch, B.M. Jesdale, J.L. Sadd, & M. Pastor (2010). Ambient air pollution exposure and full-term birth weight in 

California, Environ. Health, 9(44).

37 C. Jansen, A. Neller, G. Williams, & R. Simpson (2006). Maternal exposure to low levels of ambient air pollution 

and preterm birth in Brisbane, Australia, BJOG, 113(8): 935-941; B. Jalaludin et al. (2007). Impact of ambient air 

pollution on gestational age is modified by season in Sydney, Australia, Environ. Health, 6, 16 (2007).

38 B. Ritz et al. (2002). Ambient Air Pollution and Risk of Birth Defects in Southern California, Am. J. Epidem., 

155(1): 17-25; S.M. Gilboa et al. (2005). Relation between ambient air quality and selected birth defects, seven 

county study, Texas, 1997-2000, Am. J. Epidemiol .,162(3): 238-252; B. Hwang, & J. Jaakkola (2008). Ozone and 

other air pollutants and the risk of oral clefts, Environ. Health Perspect., 116(10): 1411-1415.

39 K.M. Mortimer, I.B. Tager, D.W. Dockery, L.M. Neas, & S. Redline (2000). The effect of ozone on inner-city 

children with asthma: identification of susceptible subgroups, Am. J. Respir. Crit. Care Med., 162(5): 1838-1845.

40 L. Trasande et al. (2013). Exploring prenatal outdoor air pollution, birth outcomes and neonatal health care 

utilization in a nationally representative sample, J. Expo. Sci. Environ. Epidemiol., 23(3): 315-21. 

41 See ISA sec. 7.5.
25

One of the subpopulations most susceptible to ozone is children. The more than 73 

million children under age 18 comprise nearly one-fourth of the U.S. population--23.2 percent. 

Of these, nearly 20 million children are under age 5.42 Children’s singular vulnerability to air 

pollution stems from their developmental stage and their behavior. Ongoing lung growth and 

development, higher relative ventilation rates, and high levels of outdoor activity mean that 

children face unique health risks from air pollution exposure.43 It is well established that children 

cannot simply be treated as small adults and require extra protection from the harmful effects of 

air pollution44- beyond what EPA has proposed. 

Children’s respiratory systems are undergoing critical stages of development that places 

them at greater risk for ozone-induced damage.

45 In fact, most of a child’s lungs will develop 

after birth until adolescence, including 80% of alveoli, the air sacs that transfer oxygen to the 

blood.46 Children’s lungs have larger surface area per kilogram of body weight compared to 

adults.47 As described by EPA, “[c]hildren are considered to be at greater risk from O3 exposure 

because their respiratory systems undergo lung growth until about 18-20 years of age and are 

therefore thought to be intrinsically more at risk for O3-induced damage.”48 In other words, 

children’s lungs continue to grow until they reach adulthood, during which time they are more 

vulnerable to damage. Children’s immune systems are also still developing, making them more 

susceptible to infection and respiratory illness than adults.49 

Children have higher baseline ventilation rates relative to lung volume and breathe in 

more air per pound of body weight.50 As a result, they take in higher relative doses of air 

pollutants than adults do. Children also tend to have a greater oral breathing contribution than 

adults, i.e., are mouth breathers, further increasing pollutant intake.51

 

42 U.S. Census Bureau (2014). Population Division, Annual Estimates of the Resident Population for Selected Age 

Groups by Sex for the United States, States, Counties, and Puerto Rico Commonwealth and Municipios: April 1, 

2010 to July 1, 2013. 

43 American Academy of Pediatrics Committee on Environmental Health, Ambient Air Pollution: health hazards to 

children (2004). Pediatrics, 114: 1699-1707. Statement was reaffirmed in 2010.

44 World Health Organization (2005). The Effects of Air Pollution on Children’s Health and Development: a review 

of the evidence E86575, available at http://www.euro.who.int/document/E86575.pdf.

45 See e.g., T.F. Bateson & J. Schwartz (2007). Children's response to air pollutant, J. Toxicol. Environ. Health, 

71(3): 238-243; C.G. Plopper & M.V. Fanucchi (2000). Do urban environmental pollutants exacerbate childhood 

lung diseases?, Environ. Health Perspect., 108(6), A252–A253; L. Trasande & G.D.Thurston (2005). The role of air 

pollution in asthma and other pediatric morbidities, J Allergy Clin. Immunol.. 115(4): 689-699.

46 R.R. Dietert et al. (2000). Workshop to Identify Critical Windows of Exposure for Children's Health: immune and 

respiratory systems workgroup summary, Environ Health Perspect., 108(supp 3), 483-490; see also J. Schwartz 

(2004). Air pollution and children’s health, Pediatrics, 113(4): 1037-1043; M. Dunnil (1962). Postnatal growth of 

the lung, Thorax, 17, 329-333.

47 Schwartz 2004, supra note 45.

48 Policy Assessment at 3-81.

49 Dietert et al. 2000, supra note 45; Bateson & Schwartz 2007, supra note 44. 

50 U.S. EPA (2011). Exposure Factors Handbook: 2011 Edition (EPA/600/R-090/052F); Wolf (ed.) (2000). Indoor 

Air Pollutants Affecting Child Health. American College of Medical Toxicology; ISA Table 4-5. 

51 W.D. Bennett, K.L. Zeman, & A.M. Jarabek (2008). Nasal contribution to breathing and fine particle deposition 

in children versus adults, J. Toxicol. Environ. Health A., 71(3): 227-237; U.S. EPA 2011, supra note 49; Wolf 2000 ̧ 

supra note 49.
26

In addition to all of these physiological factors that make children more vulnerable to 

ozone exposure, they are more likely to be active outdoors. 52 Through sports, school, and play, 

children’s outdoor activities increase their exposure to ozone pollution and, correspondingly, 

increase the likelihood that they will suffer adverse ozone-related health impacts.53 Children 

spend more time outdoors during midday and afternoons when pollutant levels tend to be higher. 

High intensity activities increase ventilation rates and pollution inhalation.54 This extra 

vulnerability is not lost on EPA, which found that “the percentages of children estimated to 

experience exposures of concern is considerably larger than the percentages estimated for adult 

populations (i.e., approximately 3-fold larger across urban study areas).”55 Playing outside and 

participating in sports and activities are important parts of growing up and encouraging healthy, 

active, and well-balanced lifestyles. Instead of forcing them to be shuttered indoors to avoid 

damage to their sensitive, developing bodies, we should be creating a safe, clean environment 

where our kids can be kids.

The evidence showing children’s physiological vulnerability to ozone exposure is strong. 

A sizeable and growing body of scientific studies demonstrates serious health harms from 

exposure to ozone concentrations at or below 60 ppb, including respiratory impacts, decreased 

pulmonary function, impaired lung development, new asthma onset, and increased respiratoryrelated hospitalization and emergency room visits. Looking at infants, a Virginia study found 

that they were at greater risk for respiratory symptoms when exposed to ozone, even with mean 

8-hour maximum concentration as low as 54.5 ppb and only exceeding 80 ppb twice during the 

study period. 

These panel studies demonstrate health impacts to children at ambient concentrations 

below what EPA proposes for the new standard. Additional studies of children at summer camp, 

where a great deal of time is spent outdoors and being active, consistently show that increasing 

levels of ozone are associated with diminished lung function. 56 Children ages 8-15 at a summer 

camp in New Jersey showed decreases in lung function associated with ozone exposure, even 

when excluding concentrations above 60 ppb.

57

 

Evidence indicates that, for some children, ozone may contribute to their development of 

incident asthma. A significant cohort study in California showed that healthy, active children 

playing three or more sports and growing up in communities with ambient ozone levels ranging 

from 55.8 to 69 ppb were over three times more likely to develop asthma than their peers in 

 

52 Proposed Rule at 75,267: “It is generally recognized that children spend more time outdoors than adults, and, 

therefore, would be expected to have higher exposure to O3 than adults”; see also U.S. EPA (2011). Health Risk and 

Exposure Assessment for Ozone (EPA-452/R-14-004a), 2-18 [hereinafter HREA]. 

53 HREA at 5-11:“Due to the increased amount of time spent outdoors engaged in relatively high levels of physical 

activity (which increases intake), school-age children as a group are particularly at risk for experiencing O3-related 

health effects.”

54 See ISA at 4-31. 

55 Proposed Rule at 75,285 (emphasis added). 

56 See P.L. Kinney, G.D. Thurston, & M. Raizenne (1996).The effects of ambient ozone on lung function in 

children: A reanalysis of six summer camp studies, Env. Health Perspect., 104(2): 170-174; G.D. Thurston, M. 

Lippmann, M.B. Scott, & J.M. Fine (1997). Summertime haze air pollution and children with asthma, Am. J. of 

Resp. and Crit. Care Med., 155(2): 654-660. 

57 Spektor et al. 1988, supra note 16.
27

communities with ozone levels ranging from 30.6 to 50.9 ppb.58 None of the high ozone 

communities would have violated a primary standard in the upper range of what EPA now 

proposes. Similarly, another noteworthy California study found that a 5 ppb increase in annual 

average 8-hour ozone concentrations resulted in positive associations with children having 

asthma and having asthma attacks, with maximum average levels of only 59.5 ppb.

59

 A study of 

Medicaid children in Harris County, Texas investigated the effect of increased short-term ozone, 

PM2.5 and nitrogen dioxide concentrations on the timing of asthma onset. Each 10 ppb increase 

in ozone was significantly associated with new-onset asthma during the warm season. The 

results indicated that among children who developed asthma, their initial date of diagnosis was 

more likely to occur following periods of higher short-term ambient pollutant levels.60 These 

studies suggest that even if communities are able to meet ozone standards within the range and 

form that EPA is proposing, more children would face greater risk for developing asthma 

compared to communities meeting a standard set at 60 ppb or below.

Children with asthma have repeatedly been shown to suffer from both lung function 

decrements and respiratory symptoms.61 Even children without asthma are suggested to be at 

higher risk for of respiratory-related pulmonary impacts than adults.62

An Atlanta study looked at emergency department visits for children under 4-years-old 

and found that each 30 ppb increase in the 3-day average of ozone was associated with an 8 

percent higher risk of pneumonia and 4 percent higher risk of upper respiratory infection.63

Another Atlanta study of children ages 5-17 found that children are particularly at risk for ozoneinduced respiratory impacts and saw a 6.4 percent increase in emergency room visits for a 30 

ppb increase in 8-hour concentrations. Mean annual 8-hour concentrations were only 47.3 ppb

and a dose-response relationship between ozone exposure and emergency room visits for 

children was evident at concentrations as low as 30 ppb.

64

 

 

58 R. McConnell et al. (2002). Asthma in exercising children exposed to ozone: A cohort study, Lancet, 359(9304): 

386-391. 

59 L.J. Akinbami, C.D. Lynch, J.D. Parker, & T.J. Woodruff (2010). The association between childhood asthma 

prevalence and monitored air pollutants in metropolitan areas, United States, 2001-2004, Environ Res., 110(3): 294-

301. 

60 J.K. Wendt, E. Symanski , T.H. Stock, W. Chan, & X.L. Du (2014). Association of short-term increases in 

ambient air pollution and timing of initial asthma diagnosis among Medicaid-enrolled children in a metropolitan 

area. Environ. Res., 131: 50-8.

61 J. Just et al., Short-term health effects of particulate and photochemical air pollution in asthmatic children, Eur. 

Resp. J., 20(4), 899-906 (2002); Mortimer et al. 2000, supra note 38; M.A. Rosset al (2002). Effect of ozone and 

aeroallergens on the respiratory health of asthmatics, Arch. of Env. Health, 57(6): 568-578; Thurston et al. 1997, 

supra note 55; I. Romieu et al. (1997). Effects of intermittent ozone exposure on peak expiratory flow and 

respiratory symptoms among asthmatic children in Mexico City, Arch. of Env. Health, 52(5): 368-376.

62 See e.g., P. Höppe et al. (2003). Environmental ozone effects in different population subgroups, Int. J. of Hygiene 

and Env. Health, 206(6): 505-516; see also ISA at 6-61: “evidence suggests that the ambient O3-associated lung 

function decrements found in children overall were not solely due to effects in children with asthma, and that 

increases in ambient O3 exposure may decrease lung function in healthy children.”

63 L.A. Darrow, M. Klein, W.D. Flanders, J.A. Mulholland, P.E. Tolbert, & M.J. Strickland (2014). Air Pollution 

and Acute Respiratory Infections Among Children 0-4 Years of Age: An 18-Year Time-Series Study, Am. J. 

Epidemiol., 180(10): 968-77.

64 M.J. Strickland et al. (2010). Short-term associations between ambient air pollutants and pediatric asthma 

emergency department visits, Am. J. of Resp. and Crit. Care Med., 182(3): 307-316.
28

A number of new studies released since EPA’s ISA was published show that rising 

ambient ozone concentrations are associated with increased hospitalizations and emergency 

room visits for children.65 Indeed, the ISA already concluded that chronic ozone exposure is 

associated with childhood asthma hospital admissions in multiple studies with mean annual 8-

hour maximum ozone concentrations of less than 41 ppb.

66 There is also evidence that chronic 

exposure to ozone may be damaging to children’s health later in life. For instance, a study of 

freshman university students in California found that lifetime exposure to high ambient ozone 

levels was associated with decreased airway function.67

For ethical reasons, controlled human exposure studies are generally performed on 

healthy adults, not children – thus resulting in a lack of exposure study data for children. That 

understandable lack of controlled exposure data has led to undervaluing risks to children by 

treating them like adults in considering the available controlled exposure data. EPA largely 

relies on a single study from 1985 with a limited sample size of 22 children, along with modeling 

and opaque references to summer camps studies, to assert that “children exhibit the same lung 

function responses following O3 exposures as healthy 18 year olds.”68 At the same time, EPA, 

agreeing with CASAC, says that“[c]ompared to the healthy individuals included in controlled 

human exposure studies, members of at-risk populations (e.g., asthmatics, children) could be 

more likely to experience adverse effects, could experience larger and/or more serious effects, 

and/or could experience effects following exposures to lower O3 concentrations.”69 Given

CASAC’s and EPA’s recognition of the clear evidence that children experience greater 

sensitivity to and impacts from exposure to ozone, EPA’s assessments need to place greater

relative value on epidemiological studies of children. 

As multiple studies cited above demonstrate, reducing ozone concentrations can reduce 

respiratory morbidity for children. CASAC has stated that exposures of 70 ppb “are of 

significant concern, especially for children, asthmatics, the elderly and other at risk 

populations.”70 Given the substantial evidence of impacts to health resulting at 8-hour 

concentrations below 65 ppb, it is inconceivable that a standard of 70 ppb or even 65 ppb would 

be protective of children. Indeed, it is questionable whether even a 60 ppb standard would 

protect children. Given the requirement to err on the side of caution, EPA should set a primary 

standard that does not exceed 60 ppb. 

 

65 See e.g., J.A. Gleason, L. Bielory, & J.A. Fagliano (2014). Associations between ozone, PM2.5, and four pollen 

types on emergency department pediatric asthma events during the warm season in New Jersey: a case-crossover 

study, Environ. Res., 32: 421-429; Darrow, supra note 62; M.J. Strickland, M. Klein, W.D. Flanders, H.H. Chang, 

J.A. Mulholland, P.E. Tolbert, & L.A. Darrow (2014). Modification of the effect of ambient air pollution on 

pediatric asthma emergency visits: susceptible subpopulations, Epidemiology, 25(6): 843-850.

66 ISA at 2-23. 

67 Tager et al. 2005, supra note 19.

68 Proposed Rule at 75,248, n. 28; see also id. at 75,275 (“In the near absence of controlled human exposure data for 

children, risk estimates are based on the assumption that children exhibit the same lung function response following 

O3 exposures as healthy 18 year olds (i.e., the youngest age for which controlled human exposure data is 

available).”).

69 Id. at 75,273.

70 Letter from CASAC Chair Dr. H. Christopher Frey to U.S. EPA Administrator Gina McCarthy re: Second Draft 

Policy Assessment for the Review of the Ozone National Ambient Air Quality Standards (EPA-CASAC-14-004), 7, 

June 26, 2014 [hereinafter CASAC Letter 2014a].
29

A focus on children is particularly appropriate because, as EPA acknowledges, “the 

percentages of children estimated to experience exposures of concern is considerably larger than 

the percentages estimated for adult populations (i.e., approximately 3-fold larger across urban 

study areas).”71 Thus, not only are children physiologically more sensitive, but they also more 

often experience levels of ozone pollution that health science indicates is likely to result in 

adverse health impacts. 

2. Asthmatics Are a Large Subpopulation Highly Sensitive to Ozone, 

Particularly Asthmatic Children 

. 

Asthma is a highly prevalent disease in the United States. About 1 in 12 people, or about 

25 million people, have asthma.72 That represents approximately 8 percent of adults, or 18.7 

million adults, and 9.3 percent of children, or 6.8 million children. 73 The Centers for Disease 

Control and Prevention (CDC) estimate that each year there are 14.2 million visits to physician 

offices, 1.3 million visits to hospital outpatient departments, and 1.8 million visits to emergency 

departments with asthma as primary diagnosis, and an estimated 3,600 deaths each year from 

asthma.74 

Air pollution is known to trigger asthma exacerbations and is associated with asthma 

symptoms, airway inflammation, airway hyperresponsiveness, decreased lung function, and 

reduced response to asthma rescue medications. Controlled studies have found that asthmatics 

experience twice the decrement in lung function of healthy people when exposed to the same 

level of ozone.75 As a 2014 review article explained in summarizing the evidence: 

The idea that outdoor air pollution can cause exacerbations of pre-existing asthma 

is supported by an evidence base that has been accumulating for several decades, 

with several studies suggesting a contribution to new-onset asthma as well.

76

The article presented a mechanistic framework, shown below, for the effects of air pollution, 

including ozone, in asthma: 

 

71 Proposed Rule at 75,272.

72 CDC, Asthma in the US, available at http://www.cdc.gov/VitalSigns/asthma (accessed Mar. 15, 2015).

73 CDC (2012). National Health Interview Survey. 

74 Id.

75 D.H. Horstman, B.A. Ball, J. Brown, T. Gerrity, & L.J. Folinsbee (1995). Comparison of pulmonary responses of 

asthmatic and nonasthmatic subjects performing light exercise while exposed to a low level of ozone. Toxicol Ind 

Health, 11 (4): 369-85.

76 M. Guarnieri & J.R. Balmes (2014). Outdoor air pollution and asthma, Lancet, 383 (9928): 1581-92.
30

Figure 1. Mechanistic framework for air pollution effects in asthma.77

The sensitivity of asthmatics to ozone exposure is particularly true for children. Asthma 

is the most common chronic disorder in children. As noted earlier, in the most recent national 

survey by the CDC, in 2012, 6.8 million children reported having asthma.78 Younger children 

are particularly affected. Almost half of all children have at least one episode of wheeze before 

age six. 48 percent of preschool children with asthma have suffered an asthma attack in the 

preceding year -- a rate higher than for any other age group.79

Young children with asthma have long been regarded as a group who are very 

susceptible to adverse effects from air pollution because of their developing lungs, 

immature metabolic pathways, high ventilation rates per body weight, and increased 

times exercising outdoors. Even exposures in utero might affect postnatal risk of asthma 

and asthma exacerbations. Low birthweight, which might be associated with narrow 

airways during early childhood, is a risk factor from symptoms of asthma related to air 

pollution.80

 

77 Id. 

78 CDC 2012, supra note 72.

79 Guarnieri & Balmes 2014, supra note 75. 

80 Id.
31

In part, asthmatic children are more highly sensitive to ozone because of the early stage 

of the physiological development of their lungs. As explained by Guamieri and Balmes: 

Children appear to be most vulnerable to the harmful effects of ambient air 

pollutants. As their lungs are not completely developed, children may experience 

greater exposure to environmental pollutants than adults and the higher doses of 

varied composition may remain in their lungs for a greater duration. Altogether, 

the negative effects of air pollutants on pulmonary function place children at a 

greater risk of air pollutant-induced exacerbation of asthma for the duration of 

their lives. 81

Indeed, there numerous studies tying increased air pollution to asthma onset and to 

triggering attacks among asthmatics. Children with asthma have repeatedly been shown to suffer 

from both lung function decrements and respiratory symptoms.82 Even children without asthma 

are suggested to be at higher risk for of respiratory-related pulmonary impacts than adults.83

Studies have documented respiratory symptoms in children with asthma such as chest 

tightness, persistent cough, and shortness of breath, even at prior-day levels of only 52.1 ppb.84

An eight-city U.S. study of inner-city children with asthma found that adverse respiratory effects 

were experienced by children across all cities, which together had a mean 8-hour average ozone 

concentration of only 48 ppb.

85 Ozone was found to be associated with significant declines in 

pulmonary function and asthma symptoms in the children examined. Another analysis of the 

same group found that even when excluding the 5 percent of days where ambient concentrations 

exceeded 80 ppb, results were nearly identical.86 Another key study showed lung decrements in 

children ages 7-13 following exposure to 8-hour concentrations of less than 51 ppb.

87

 Still 

another study of French children with asthma revealed both decreases in lung function and 

respiratory symptoms (asthma attacks and respiratory infections) at maximum concentrations of 

61.7 ppb.

88” 

There is also evidence that long-term, chronic ozone exposure may be associated with 

children’s hospital visits. For example, a New York State study showed that long-term ozone 

 

81 L. Tzivian (2011). Outdoor air pollution and asthma in children, J. Asthma, 48 (5): 470-81.

82 Just et al. 2002, supra note 60; Mortimer et al. 2000, supra note 38; M.A. Ross. et al. (2002). Effect of ozone and 

aeroallergens on the respiratory health of asthmatics, Arch. of Env. Health, 57(6): 568-578; Thurston, G.D., 

Lippmann, M., Scott M.B., & Fine, J.M. (1997). Summertime haze air pollution and children with asthma, Am. J. of 

Resp. and Crit. Care Med., 155(2), 654-660; I. Romieu et al. 1997, supra note 60.

83 See e.g., P. Höppe et al., supra note 66; see also ISA at 6-61: “evidence suggests that the ambient O3-associated 

lung function decrements found in children overall were not solely due to effects in children with asthma, and that 

increases in ambient O3 exposure may decrease lung function in healthy children.”

84 J.F. Gent et al. (2003). Association of Low-Level Ozone and Fine Particles with Respiratory Symptoms in 

Children with Asthma. JAMA, 290(1): 1859-1867.

85 Mortimer et al. 2000, supra note 38.

86 K.M. Mortimer, L.M. Neas, D.W. Dockery, S. Redline, & I.B. Tager (2002). The effect of air pollution on innercity children with asthma. Eur. Respir. J., 19(4): 699–705.

87 M.H. Gielen, S.C. van der Zee, J.H. van Wijnen, C.J. van Stehen, & B. Brunekreef (1997). Acute effects of

summer air pollution on respiratory health of asthmatic children, Am. J. Respir. Crit. Care Med., 155(6): 2105-2108.

88 Just et al. 2002, supra note 60.
32

exposure was associated with first asthma hospital admissions for children 1-to 6-years-old. 89

Thus, children exposed to chronically high ozone levels were more likely to develop asthma 

exacerbations so severe as to require hospitalization. Just a 1 percent increase in mean ozone 

concentrations during the ozone season increased the risk of a child’s hospital admission by 22 

percent. Notably, ozone levels weren’t actually all that high - annual mean 8-hour concentrations 

were only 41.06 ppb and only 50.62 ppb during the ozone season. Younger children and those in 

low socioeconomic groups showed a greater risk of asthma hospitalization than did other 

children at the same ozone levels.

A study of primarily African-American, Latino, and lower-income children with asthma 

in Detroit, Michigan explored the question of how ambient air pollution affects susceptible 

populations. Corticosteroid use was used as a marker of more severe asthma. Daily one-hour 

maximum ozone concentrations were associated with increased odds of respiratory symptoms, 

particularly among children using corticosteroid medication and among children living in the 

southwest community of Detroit. Similar patterns of associations were not seen with PM. 

Researchers concluded that ozone at levels near or below annual standard levels are associated 

with negative health impact in this population of asthmatic children.90 Researchers in Pittsburgh, 

Pennsylvania used a case-crossover approach to investigate the relationship of air pollution and 

emergency department visits in an urban population. A 2.5 percent increase was observed in 

asthma emergency department visits for each 10 ppb increase in the 1-hour maximum ozone 

level on day two. 91 

The relationship between ozone and respiratory impacts in children is further supported 

by connections between ozone exposure and respiratory-related hospital admissions and 

emergency room visits, as well as increased asthma medication use. Epidemiological studies 

linking ozone exposure to respiratory-related hospitalizations and emergency room visits for 

children offer important evidence of some of the more severe impacts that ozone has on 

children’s health and well-being. 

For instance, a New York City study showed stronger associations between ozone 

exposure and asthma-related hospital admissions for 6- to 18-year-olds, whose lungs are still 

developing, compared with other age groups.1 Another study in Seattle demonstrated higher 

asthma hospitalizations for children under age 18 than for adults, which the authors found 

“suggests that children are more immediately responsive to adverse effects of O3 exposure.”1In 

it, a 30 ppb increase in 8-hour maximum ozone concentrations was associated with a 19.1-36.8 

percent increase in asthma emergency-department visits for children. A Canadian study also 

showed stronger associations between asthma-related emergency room visits and ozone exposure 

in 5- to 14-year-olds than for any other age group.

92 A study of children with asthma under age 

12 in Connecticut and Massachusetts found that ozone levels were significantly associated with 

 

89 S. Lin, X. Liu, L.H. Le, & S. Hwang (2008). Chronic exposure to ambient ozone and asthma hospital admissions 

among children, Env. Health Perspect., 116(12): 1725-1730.

90 T.C. Lewis et al. (2013). Air pollution and respiratory symptoms among children with asthma: vulnerability by 

corticosteroid use and residence area, Sci.Total Environ., 448: 48-55.

91 J.A. Glad et al. (2012). The relationship of ambient ozone and PM(2.5) levels and asthma emergency department 

visits: possible influence of gender and ethnicity, Arch Environ Occup Health, 67(2), 103-8.

92 Villeneuve et al. (2007). Outdoor air pollution and emergency department visits for asthma among children and 

adults: A case-crossover study in northern Alberta, Canada, Env. Health, 6(40).
33

respiratory symptoms and rescue medication use among children.93 Maximum eight-hour 

concentrations of only 63.3 ppb were associated with a 30 percent increase in chest tightness, 

while previous day levels of 52.1 ppb or higher were associated with increased chest tightness, 

persistent cough, and shortness of breath.

New studies provide extensive further evidence that people with respiratory disease are at

increased risk, above that faced by the general population. Critical new evidence since the last 

review correlates exposure to ozone with respiratory symptoms, increased airway 

responsiveness, school absenteeism, and increased medication use in people with asthma.

A study sought to establish the prevalence of “responders” in four different population 

subgroups: children, asthmatics, the elderly, and athletes, by assessing symptoms and measuring 

respiratory function.94 The study found higher rates of ozone responders in asthmatics (21 

percent) and children (18 percent), as compared to the elderly and athletes (both 5 percent). This 

means that children and asthmatics have a higher risk of being ozone sensitive and experiencing 

more acute lung function decrements than these other population groups. This study indicates

that individuals with asthma are more sensitive to the effects of low-level ozone exposures than 

healthy persons.

Important new evidence of the increased sensitivity of children with asthma comes from 

two studies by Mortimer et al.95 The effects of daily ambient air pollution were examined in a 

cohort of 864 asthmatic children in 8 urban areas of the U.S. in a longitudinal study. The cities 

studied were Baltimore, Chicago, Cleveland, Detroit, Bronx/East Harlem, St. Louis, and 

Washington D.C. Eight-hour average ozone concentrations from 10 a.m. to 6 p.m. were 48 ppb. 

Median concentrations across cities ranged from 34 to 58 ppb. Researchers found that 

summertime air pollution at levels below the current air quality standards was significantly 

related to symptoms and decreased pulmonary function in children with asthma. Ozone was most 

influential on peak expiratory flow rate. Adverse respiratory effects were observed in all cities. 

This compelling study provides strong support for an 8-hour ozone standard of 60 ppb or below.

Another study of the same cohort found that asthmatic children born prematurely or with 

low birth weight have the greatest response to ozone.96 Scientists sought to ascertain which 

subgroups in a cohort of 846 inner-city asthmatic children aged 4-9 years old were most 

susceptible to the effects of summertime ozone. Children were recruited from emergency 

departments and primary care clinics the eight U.S. cities. The mean 8-hour ozone concentrations 

from 10 a.m. to 6 p.m. across these cities were 48 ppb. The study reported that “children of low 

birth weight or of premature birth are at greater risk for respiratory problems, and appear to be 

substantially more susceptible to the effects of summer air pollution than children of normal birth 

weight or full-term gestation.” 

 

93 Gent, J.F., et al. (2003). Association of Low-Level Ozone and Fine Particles with Respiratory Symptoms in 

Children with Asthma. JAMA, 290(1): 1859-1867

94 P. Höppe et al. (2003). Environmental ozone effects in different population subgroups, Int. J. of Hygiene and Env. 

Health, 206(6): 505-516.

95 Mortimer et al. 2000, supra note 38. 

96 Mortimer et al. 2002, supra note 85.
34

3. Adult “Responders” Are a Sensitive Population that Must Be 

Protected Under the Revised Standard

It has long been known that among healthy adults, some people are especially sensitive to 

ozone exposures. These people, historically known as responders, experience a markedly 

increased decline in pulmonary lung function in response to exposure to ozone, and their 

elevated responses are consistent over time. The controlled human exposure studies demonstrate 

that, within even a small sample of the population, some of those individuals respond with 

greater adverse effect to the ozone exposure.97 A high level of inter-individual variability is also 

evidenced by the 3- to 20-fold difference in airway inflammation following ozone exposure.98 In 

this review, for the first time, EPA recognizes that a certain genetic makeup predisposes some 

individuals to be especially responsive to ozone exposures, although other characteristics may 

also play a role that is not currently clear. It is estimated that between 5 and 20 percent of the 

healthy population are responders.99 It is imperative that the standards be set at levels that will 

protect these responders, and not merely at levels that will protect the population on average.

4. Outdoor Workers, Due to Their Prolonged Exposures to Ambient Air, 

Are a Sensitive Population Requiring Heightened Protection

Another large and important subpopulation with heightened vulnerability to ozone is 

outdoor workers. Outdoor workers experience more frequent exposure to ozone than the general 

population, due to the time spent outdoors, and the increased breathing rate under physical 

exertion. Several studies have examined the association between ozone exposure and health 

outcomes in outdoor workers, including farm workers,100 mail carriers,

101 and others.102

 In the 

United States, this population constitutes more than 9 million people. Outdoor workers include a 

diverse set of occupations, ranging from construction workers to farm workers. Table 1 lists 

some categories of outdoor workers and provides estimates of population size though this 

tabulation does not include members of the military forces. 

Table 1. Worker Counts for Occupations likely to Involve Outdoor Work.

103

Occupations Number of workers

 

97 C.S. Kim et al. (2011). Lung function and inflammatory responses in healthy young adults exposed to 0.06 ppm 

ozone for 6.6 hours, Am. J. Respir. Crit. Care Med.,183(9): 1215-21.

98 Proposed Rule at 75,247.

99 U.S. Environmental Protection Agency. Office of Air Quality Planning and Standards. Review of the National 

Ambient Air Quality Standards for Ozone Preliminary Assessment of Scientific and Technical Information. Draft 

Staff Paper November 1988.

100 Brauer et al. 1996, supra note 17.

101 C. Chan & T. Wu (2005). Effects of ambient ozone exposure on mail carriers’ peak expiratory flow rates,

Environ Health Perspect, 113: 735-738.

102 Tovalin, et al. (2006). DNA damage in outdoor workers occupationally exposed to environmental air pollutants, 

Occup. Environ. Med., 63: 230-236; M.S. O'Neill et al. (2003). Ozone exposure among Mexico City outdoor 

workers, J. Air Waste Manag. Assoc., 53: 339-346.

103 Derived from Census 2000 EEO Data Tool, available at http://www.census.gov/eeo2000/index.html. The Census 

Bureau tabulation excludes the four military categories and 35 occupational categories falling below a 10,000 person 

threshold. 
35

Farm, Ranch, and Other Agricultural Managers 201,980

Farmers and Ranchers 587,015

Construction Managers 651,400

Surveyors, Cartographers, and Photogrammetrists 35,640

Surveying and Mapping Technicians 82,180

Conservation Scientists and Foresters 28,340

Athletes, Coaches, Umpires, and Related Workers 194,120

Emergency Medical Technicians and Paramedics 112,885

Fire Fighters 242,395

Miscellaneous Law Enforcement Workers 9,250

Police Officers 597,925

Crossing Guards 55,070

Lifeguards and Other Protective Service Workers 98,560

First-Line Supervisors/Managers of Landscaping, Lawn Service, and 

Groundskeeping Workers

134,200

Grounds Maintenance Workers 1,014,820

Door-To-Door Sales Workers, News and Street Vendors, and 

Related Workers

195,650

Couriers and Messengers 203,545

Meter Readers, Utilities 43,400

Postal Service Mail Carriers 354,395

Miscellaneous Agricultural Workers, Including Animal Breeders 806,075

Fishing and Hunting Workers 51,100

Forest and Conservation Workers 18,980

Logging Workers 105,675

Brickmasons, Blockmasons, and Stonemasons 212,210

Cement Masons, Concrete Finishers, and Terrazzo Workers 94,500

Construction Laborers 1,266,235

Miscellaneous Construction Equipment Operators 357,330

Roofers 222,995

Fence Erectors 29,835

Hazardous Materials Removal Workers 22,425

Highway Maintenance Workers 96,185

Rail-Track Laying and Maintenance Equipment Operators 12,200

Septic Tank Servicers and Sewer Pipe Cleaners 8,175

Miscellaneous Construction and Related Workers 33,505

Derrick, Rotary Drill, and Service Unit Operators, and Roustabouts, 

Oil, Gas, and Mining 

15,545

Earth Drillers, Except Oil and Gas 29,140

Explosives Workers, Ordnance Handling Experts, and Blasters 9,590

Aircraft Mechanics and Service Technicians 183,075

Electrical Power-Line Installers and Repairers 106,285

Railroad Brake, Signal, and Switch Operators 10,070

Railroad Conductors and Yardmasters 48,330
36

Parking Lot Attendants 62,420

Service Station Attendants 126,575

Transportation Inspectors 39,945

Miscellaneous Transportation Workers, Including Bridge and Lock 

Tenders and Traffic Technicians 

20,650

Pumping Station Operators 19,395

Refuse and Recyclable Material Collectors 88,455

TOTAL NUMBER OF WORKERS 8,939,670

In addition to the outdoor workers discussed above, recreational exercising adults and 

children will experience increased ozone exposure due to increased breathing rates.104 Because 

participation in some sports can result in a child drawing up to 17 times the “normal” amount of 

air into the lungs, young athletes may be more likely to develop asthma.105 Hikers, bikers, 

walkers, runners, and those that play outdoor sports are also at risk because their increased 

ventilation rate exposes them to a higher dose of ozone. 

5. The Elderly Are Also a Large Sensitive Subpopulation At Risk From 

Ozone

The elderly are another sensitive subpopulation at risk from ozone exposure, as identified 

by EPA. More than 14.1 percent of the U.S. population is age 65 or older, equal to nearly 45 

million elderly people.106 The elderly are vulnerable to ozone exposure due to decreased 

physiological, metabolic, and compensatory processes, and a greater incidence of cardiovascular 

and respiratory disease, compared to younger adults. For example, one meta-analysis of 

epidemiologic evidence regarding sensitivity to mortality or hospital admission from short-term 

ozone exposure found persuasive evidence of increased mortality risk for elderly populations.107 

Similarly, studies from other countries report a pronounced relationship between daily mortality 

and ozone exposure in elderly108 and that ozone exposure increases hospital admission rates in 

the elderly. 

6. Recent Evidence Also Suggests New Subpopulations with Heightened 

Sensitivity to Ozone

The 2013 ISA includes new categories of populations at risk that were not identified in 

previous reviews. For example, two new categories are individuals with reduced intake of 

certain nutrients (i.e., vitamins C and E), and individuals with certain genetic makeup, including 

variations in genes related to oxidative metabolism or inflammation. While there are no ready 

estimates of the numbers of people that fall within these two categories, the expansion of EPA’s 

 

104 Brunekreef et al. 1994, supra note 16; Spektor et al. 1998, supra note 16; Kinney et al. 1996, supra note 55. 

105 McConnell et al. 2002, supra note 22.

106 U.S. Census Bureau, Population Division (2014). Annual Estimates of the Resident Population for Selected Age 

Groups by Sex for the United States, States, Counties, and Puerto Rico Commonwealth and Municipios: April 1, 

2010 to July 1, 2013.

107 M.L. Bell, A. Zanobetti, & F. Dominici (2014). Who is more affected by ozone pollution? A systematic review 

and meta-analysis. Am. J. Epidemiol., 180 (1): 15-28.

108 S. Cakmak, R.E. Dales, & C.B. Vidal (2007). Air pollution and mortality in Chile: susceptibility among the 

elderly. Environ. Health Perspect., 115: 524-527.
37

populations at risk indicates that more people may be at risk of ozone and need stronger 

standards than were adopted in 2008. 

C. Ozone Can Pose Significant Health Risks for Populations with Pre-Existing 

Health Conditions

 

Substantial and growing evidence warns that people with an array of pre-existing 

conditions such as obesity, diabetes, heart disease, COPD, and cystic fibrosis may be at increased 

risk from exposure to ozone. The ISA now recognizes a likely causal relationship between shortterm exposures to ozone and cardiovascular effects. It necessarily follows that people with heart 

disease and high blood pressure already are at increased risk from ozone exposure. The ISA also 

concludes that there is suggestive evidence that ozone causes reproductive and developmental 

effects. This being the case, pregnant women should be considered among those with increased 

susceptibility to ozone air pollution. 

1. Obesity is a Pre-Existing Condition Requiring Additional Protection 

Under the Revised NAAQS

There is growing information identifying obesity as a potential risk factor for increased 

susceptibility to ozone air pollution. More than 1 in 3 adults are considered to be obese, while 1 

in 20 adults (6.3 percent) are classified as having extreme obesity.109 Among children ages 2 to 

19, 16.9 percent are considered to be obese.110 All told, there are 80 million obese adults, and 12 

million obese children. This demographic must be carefully considered and a precautionary 

approach taken to ensure they are adequately protected. 

Obese individuals have higher breathing rates, which can increase their exposure to 

ozone and other air pollutants.111 Scientific studies have recognized obesity as a risk factor in 

asthma.112 Obesity may modify airway inflammation, which affects the sensitivity of the lung to 

ozone and obese individuals may have lower baseline lung function.113

The recently published results from the Framingham Heart Study, report that obese 

people had a larger decrease in FEV1

114 in association with previous-day ozone exposure than 

non-obese participants. The association per 10 ppb of ozone was more than twice as large for 

 

109

 K.M. Flegal, M.D. Carroll, B.K. Kit, & C.L. Ogden (2012). Prevalence of obesity and trends in the distribution 

of body mass index among US adults, 1999-2010. J. Am. Med. Assn. 301(5): 491-497; Weight Control Information 

Network, National Institute of Diabetes and Digestive and Kidney Diseases, Overweight and Obesity Statistics, 

available at http://win.niddk.nih.gov/statistics (accessed Mar. 15, 2015).

110 C.L. Ogden, M.D. Carroll, B.K. Kit, & K.M. Flegal (2012). Prevalence of obesity and trends in body mass index 

among US children and adolescents, 1999-2010, J. Am. Med. Assn. 301(5): 483-90.

111 P.D. Koman (2012). How Does the Obesity Epidemic Affect Risk from Air Pollution? Risk Science Center 

Occasional Papers, University of Michigan School of Public Health; P. Brochu, M. Bouchard, & S. Haddad (2013). 

Physiological Daily Inhalation Rates for Health Risk Assessment in Overweight/Obese Children, Adults, and 

Elderly, Risk Analysis.

112 O. Sideleva & A.E. Dixon (2014). The many faces of asthma in obesity, J. Cell. Biochem., 115 (3): 421-6.

113 A.E. Dixon et al. (2010). An official American Thoracic Society Workshop report: obesity and asthma, Proc. Am. 

Thorac. Soc., 7(5): 325-35.

114 FEV1 (forced expiratory volume in one second) is a commonly-used metric for assessing respiratory health.
38

obese subjects, compared with the non-obese.115 Similar results were reported in the Normative 

Aging Study, which found that obesity worsened the effect of ozone on lung function in the 

elderly.116 These findings are backed up by experimental studies which have found that the 

inhaled dose of ozone was greater in obese mice and that airway hyperresponsiveness and airway 

inflammatory responses to ozone were enhanced in obese mice compared to lean or normalweight mice.117 More recently, a multi-city study in China reported that the effects of ozone air 

pollution on hypertension were greatest among obese men,118 while a study of Chinese children 

reported that respiratory health effects are enhanced among obese children.119 

2. Diabetes is a Pre-Existing Condition Requiring Additional Protection

Another growing segment of the population, individuals suffering from diabetes may also 

be at greater risk of adverse health impacts from ozone exposure. According the American 

Diabetes Association, in 2012, 29.1 million Americans, or 9.3 percent of the population had been 

diagnosed with diabetes, including 208,000 people under the age of twenty.120 

A study in Santiago, Chile tested the association between daily air pollution 

concentrations and hospitalizations for serious complications of diabetes. Ozone was associated 

with increased risk of acute complications of diabetes requiring hospitalization, suggesting that 

improvements in air quality may reduce morbidity from diabetes.121 Similarly, a panel study in 

Chapel Hill, North Carolina examined the short-term effects of temperature and ozone on 

endothelial dysfunction in people with type II diabetes. Investigators reported an association 

between temperature decreases and ozone increases on endothelial dysfunction in individuals 

with diabetes.122

Laboratory toxicology studies have explored the mechanisms by which ozone might 

induce glucose intolerance and potentially lead to diabetes, though this is in the early stages of 

research. A laboratory study in rats, to be published in the journal Diabetes, reported that ozone 

plays a causative role in the development of insulin resistance, suggesting that it could boost the 

development of diabetes.123 A 2013 publication reported “acute ozone exposure induces marked 

 

115 M.B. Rice, et al. (2013). Short-term exposure to air pollution and lung function in the Framingham Heart Study, 

Am. J. Respir. Crit. Care Med., 188(11): 1351-7.

116 S.E. Alexeeff, et al. (2007). Ozone exposure and lung function: effect modified by obesity and airways 

hyperresponsiveness in the VA normative aging study, Chest, 132 (6): 1890-7.

117 R.A. Johnston et al. (2008). Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and 

enhances ozone-induced pulmonary inflammation, J. Appl. Physiol., 104: 1727–1735.

118 Y. Zhao et al. (2013). Does obesity amplify the association between ambient air pollution and increased blood 

pressure and hypertension in adults? Findings from the 33 Communities Chinese Health Study, Int. J. Cardiol., 168 

(5): e148-50. 

119 G.H. Dong et al. (2013). Obesity enhanced respiratory health effects of ambient air pollution in Chinese children: 

the Seven Northeastern Cities study, Int. J. Obes. (Lond), 37 (1): 94-100.

120 American Diabetes Association, Statistics About Diabetes-Statistics About Diabetes Data from the National 

Diabetes Statistics Report, available at http://www.diabetes.org/diabetesbasics/statistics/#sthash.1JKw9Pf7.dpufhttp://www.diabetes.org/diabetes-basics/statistics/#sthash.1JKw9Pf7.dpuf.

121 R.E. Dales, S. Cakmak, C.B. Vidal, & M.A. Rubio (2012). Air pollution and hospitalization for acute 

complications of diabetes in Chile, Environ. Int., 46: 1-5.

122 S. Lanzinger et al. (2014). The impact of decreases in air temperature and increases in ozone on markers of 

endothelial function in individuals having type-2 diabetes, Environ. Res., 134: 331-8.

123 R.E. Vella et al. (2014). Ozone exposure triggers insulin resistance through muscle c-Jun N-terminal Kinases 
39

systemic metabolic impairments in Brown Norway rats of all ages, likely through sympathetic 

stimulation.”124 These and other studies indicate that people with diabetes should be among those 

considered especially vulnerable to ozone exposures. 

3. COPD is a Pre-Existing Condition Necessitating Additional 

Protection under the Revised Standard

The ISA indicates that ozone causes adverse respiratory health effects, but it finds 

evidence inadequate to classify people with chronic obstructive pulmonary disease (COPD), a 

disease that includes both chronic bronchitis and emphysema, at increased risk from ozone. This 

is counterintuitive, because the causal finding is based in part on evidence of increased risk of 

hospital admissions, emergency room visits, and increased risk of premature death. COPD is the 

third leading cause of death in America, claiming the lives of 134,676 Americans in 2010.

125

 In 

2011, 12.7 million U.S. adults were estimated to have COPD.126 However, close to 24 million 

U.S. adults have evidence of impaired lung function, indicating an under-diagnosis of COPD.127

Studies show that people with COPD are especially susceptible to ozone. A very large 

case-crossover study of Medicare recipients in 36 U.S. cities evaluated the effect of ozone and 

PM10 on respiratory hospital admissions in the elderly over a 13-year period. The study found 

that the risk of daily hospital admissions for COPD and pneumonia increased with short-term 

increases in ozone concentrations during the warm season, but not during the cold season. 

Importantly, 8-hour mean warm season ozone concentrations in this study ranged from 15 ppb in 

Honolulu to 63 ppb in Los Angeles. As indicated in Table 2 below, ozone concentrations in most 

cities were in the 40-55 ppb range.128 This study provides powerful evidence for a standard of 60 

ppb or below. 

Table 2: Mean ozone levels in U.S. cities during 1986-1999.129

 

(JNKs) activation, Diabetes. Epub ahead of print. 

124 V. Bass et al. (2014). Ozone induces glucose intolerance and systemic metabolic effects in young and aged 

Brown Norway rats, Toxicol. Appl .Pharmacol., 273(3): 551-60.

125 Centers for Disease Control and Prevention (2013). National Center for Health Statistics. National Vital Statistics 

Report. Deaths: Final Data for 2010; 61(04).

126 CDC (2011). National Center for Health Statistics. National Health Interview Survey Raw Data, 2011. Analysis 

performed by the American Lung Association Research and Health Education Division using SPSS and SUDAAN 

software.

127 CDC (2002). Chronic Obstructive Pulmonary Disease Surveillance – United States, 1971-2000. Morbidity and 

Mortality Weekly Report. 51(SS06):1-16. 

128 M. Medina-Ramón, A. Zanobetti, & J. Schwartz (2006). The Effect of Ozone and PM10 on Hospital Admissions 

for Pneumonia and Chronic Obstructive Pulmonary Disease: A National Multicity Study, Am. J. of Epid, 163: 579-

588.

129 Id. 
40

A study in Hong Kong examined the relationship between levels of ambient air pollutants 

and the hospitalization rate due to COPD in Hong Kong. Significant effects were found between 

hospital admissions for COPD and all five ambient air pollutants examined, but ozone was the 

most important of the air pollutants studied. This study provides further evidence of the special 

susceptibility of people with COPD to ozone.130 

 

130 Ko et al. (2007). The temporal relationship between air pollutants and hospital admissions for chronic obstructive 

pulmonary disease in Hong Kong, 62(9): 780-5.
41

Likewise, a study in Taipei, Taiwan also reported positive associations between ozone 

and hospital admissions for COPD in single- and two-pollutant models, where mean ozone 

concentrations were 20.52 ppb, and maximum ozone concentrations were 62.79 ppb.

131 A French 

study reported that ozone exacerbates symptoms in COPD patients. Thirty-nine senior adults 

with severe COPD were followed by their physicians in Paris, France, during a 14-month period. 

Daily levels of PM10, ozone, sulfur dioxide, and nitrogen dioxide were monitored. Only the 8-

hour average ozone concentration was associated with exacerbation of COPD symptoms.132

According to the researchers: 

Our results are consistent with those of toxicological studies that have shown the 

inflammatory mechanisms of O3. The recruitment of inflammatory cells into the 

lung presents a risk of tissue damage through the release of toxic mediators by 

activated inflammatory cells. Perhaps this phenomenon would be more serious 

among patients suffering from COPD, in whom a pre-existent inflammation of the 

small or large airways would be constant.133

Another just published study, this one of 1,200 people with emphysema who had 

undergone lung volume reduction surgery, assessed the association between short- and long-term 

pollutant concentrations and changes in pulmonary function.134 Air pollution exposure (PM2.5 

and ozone) was strongly associated with worsened respiratory function and symptoms. 

Researchers concluded that “exposures even below those of air quality standards may still pose 

significant risks to severe chronic obstructive pulmonary disease (COPD) subjects.”135

4. Heart Disease is a Pre-Existing Condition that Poses Additional Risks 

When Exacerbated by Ozone Exposure 

EPA must also assure that the primary standard prevents adverse effects to cardiovascular 

health from ozone exposure. Heart disease is the leading cause of death for both men and women 

in the U.S. Approximately 85.6 million people in this country suffer from some form 

of cardiovascular disease, including high blood pressure.136 The ISA found that that the 

relationships between short-term exposures to ozone and both total mortality and cardiovascular 

effects are likely to be causal. ISA 1-7 to -8. There is substantial support for this finding.

Just this year, an expert consensus document prepared on behalf of the European Society 

of Cardiology explored the mechanisms of interactions and relationships between ambient air 

pollution and cardiovascular disease. As illustrated in Figure 2 below, the paper identifies 

 

131 C.Y. Yang & C.J. Chen (2007). Air pollution and hospital admissions for chronic obstructive pulmonary disease 

in a subtropical city: Taipei, Taiwan, J. Toxicol. Environ. Health, 70, 1214-1219. 

132 H. Desqueyroux, J.C. Pujet, M. Prosper, Y. Le Moullec, & I. Momas (2002). Effects of Air Pollution on Adults 

With Chronic Obstructive Pulmonary Disease, Arch. of Environ. Health, 57: 554-560. 

133 Id.

134 M. Kariisa et al. (2015). Short- and long-term effects of ambient ozone and fine particulate matter on the 

respiratory health of chronic obstructive pulmonary disease subjects, Arch. Environ. Occup. Health, 70 (1): 56-62.

135 Id. 

136 John Hopkins Medicine, Cardiovascular Disease Statistics, available at 

http://www.hopkinsmedicine.org/healthlibrary/conditions/cardiovascular_diseases/cardiovascular_disease_statistics

_85,P00243 (accessed Mar. 15, 2015).
42

multiple pathways by which air pollution is linked to cardiovascular morbidity and mortality, 

including the induction of oxidative stress, systemic inflammation, endothelial dysfunction, 

atherothrombosis, and arrhythmogenesis.137 

Figure 2. Mechanistic effects of air pollution on cardiovascular morbidity and mortality.138

The authors concluded that “[a]ir pollution should be viewed as one of several major 

modifiable risk factors in the prevention and management of cardiovascular disease.”139

Similarly, Zanobetti and Schwartz examined associations between “long-term” ozone exposures 

and survival of Medicare participants in 105 major U.S. cities who have been hospitalized for 

COPD, diabetes, congestive heart failure, and myocardial infarction. The analysis found 

significant associations between annual summer-average levels of ozone and deaths for all of 

these four groups. It finds a 6 to 8 percent increase in risk per 5 ppb increase in the summer 

average of daily maximum 8-hour ozone levels. This study provides additional support for 

considering patients with COPD, diabetes, and heart disease as susceptible populations.140 

Several recent studies published since the ISA have reported that ozone pollution 

increases risk of cardiac arrest. A case-crossover study in Houston examined emergency medical 

services data on out-of-hospital cardiac events relative to air pollution concentrations. 

Investigators reported consistent evidence of an association between out-of-hospital cardiac 

events and exposure to ozone. A 20 ppb ozone increase in the 8-hour average daily maximum 

ozone concentrations was associated with an increased risk of a cardiac event on the same day. 

 

137 D.E. Newby et al. (2015). Expert position paper on air pollution and cardiovascular disease. Eur. Heart. J., 36 

(2): 83-93.

138 Id. 

139 Id.

140 A. Zanobetti & J. Schwartz (2011). Ozone and survival in four cohorts with potentially predisposing diseases, 

Am. J. Respir. Crit. Care. Med., 184(7): 836-41; Teng et al. (2014). A systematic review of air pollution and 

incidence of out-of-hospital cardiac arrest, J. Epidemiol. Comm Health, 68 (1): 37-43.
43

Similarly, a 20 ppb increase in ozone in the previous 1 to 3 hours was also associated with an 

increased risk of a cardiac event on the same day. Mean hourly ozone concentrations in this 

study were 25.5 ppb.141 A recent study examined over 2,000 cases of out-of-hospital cardiac 

arrest in Helsinki, Finland, for the period of 1998 to 2006. Ozone pollution was linked with a 

large increase in the risk of cardiac arrest due to arrhythmia, occurring two to three days after 

exposure to ozone.142 

A 2014 study in Stockholm, Sweden used ten years of data from the Swedish cardiac 

arrest register with a time-stratified case-crossover design to analyze exposure to air pollution 

and the risk of out-of-hospital cardiac arrest. Exposure to ozone, PM2.5, PM10, NO2, and NOx

was defined as the mean urban background level during 0–2, 0–24, and 0–72 hours before the 

event and control time points. The study, which adjusted for temperature and relative humidity, 

found that ozone in urban background was associated with an increased risk of out-of-hospital 

cardiac arrest for all time windows analyzed.143 The mean 8-hour maximum ozone concentration 

in urban areas during the warm season was 34 ppb. The study suggested that short-term 

elevations of ozone urban background levels are associated with an increased risk of out-ofhospital cardiac arrest with no indication of a threshold, in a region with ∼50 μg/m3

[23.4 ppb] 

annual ozone levels. 

5. Evidence Connects Ozone Exposure to Strokes

There is also increasing evidence of a relationship between ozone exposure and stroke. A 

time-stratified case-crossover analysis evaluated the relationships between stroke hospital 

admissions and ozone among patients aged 65 years and older in Allegheny County, 

Pennsylvania. The study found that same day exposures to ozone may increase the risk of 

hospitalization for stroke, and that effects were greater in males than in females. Researchers 

concluded that “results suggest that O3 has an adverse effect on stroke hospitalization. Specific 

patient subgroups, such as males, may be at increased risk.”144 Given the growing evidence, EPA 

needs to follow the requirement of including a margin of safety to protect heart patients from 

increased risk of cardiac arrest and stroke. Indeed, such patients should be considered a sensitive 

population. 

6. Transplant Recipients Are a Sensitive Subpopulation for Ozone 

Exposure

Similarly, two studies indicate that transplant recipients may be a sensitive 

subpopulation. Not surprisingly, research suggests lung transplant patients are susceptible to 

harm from pollution. For example, a retrospective cohort study of kidney transplant recipients 

with numerous known risk factors explored whether they may constitute a sensitive subgroup as 

 

141 K.B. Ensor, l.H. Raun, & D. Persse (2013), A case-crossover analysis of out-of-hospital cardiac arrest and air 

pollution. Circulation, 127 (11): 1192-9.

142 F.S. Rosenthal et al. (2013). Association of ozone and particulate air pollution with out-of-hospital cardiac arrest 

in Helsinki, Finland: evidence for two different etiologies, J. Expo. Sci. Environ. Epidemiol., 23 (3): 281-8. 

143 A. Raza et al. (2014). Short-term effects of air pollution on out-of-hospital cardiac arrest in Stockholm, Eur. 

Heart J., 35 (13): 861-8.

144 X. Xu, Y. Sun, S. Ha, E.O. Talbott, & C.T. Lissaker (2013). Association between ozone exposure and onset of 

stroke in Allegheny County, Pennsylvania, USA, 1994-2000, Neuroepidemiology, 41(1): 2-6.
44

far as air pollution is concerned. Monthly concentrations of ozone and PM10 were calculated 

from ambient monitoring data and interpolated to zip code centroids according to patients' 

residence. For the entire transplant cohort, average pollutant levels for ozone were 25.5 ± 4.4 

ppb. For each 10 ppb increase in ozone, the risk of fatal coronary heart disease increased by 

about 34 percent in both the single and the two pollutant model. Researchers concluded that for 

kidney transplant recipients, ambient ozone levels are potentially associated with higher risk of 

fatal coronary heart disease.145 

A retrospective cohort study of 397 bilateral lung recipients examined the relation 

between ambient air pollution, chronic lung allograft dysfunction, and mortality.146 These studies 

suggest that transplant recipients may be at increased risk for chronic lung allograft dysfunction

from ozone exposures and should be considered a susceptible population. 

7. Cystic Fibrosis is a Pre-Existing Condition Requiring a More 

Protective Ozone Standard

People with cystic fibrosis, a chronic lung disease, may also be at risk. Cystic fibrosis is 

a disease that causes thick, sticky mucus to form in the lungs, pancreas, and other organs. This 

mucus clogs the lungs causing wheezing, shortness of breath, and frequent lung infections.147

Cystic fibrosis involves significant inflammation and oxidative stress, and exposure to air 

pollutants can worsen the lung damage. Deficits in innate immunity, chronic infection, oxidative 

stress, and inflammation due to cystic fibrosis may indicate a population disproportionately 

vulnerable to the harms of air pollution. The Cystic Fibrosis Foundation estimates that 30,000 

children and adults in the U.S. have cystic fibrosis.148

A study in São Paulo, Brazil investigated the association between the short-term variation 

in the concentration of air pollutants and the occurrence of respiratory exacerbations in children 

and adolescents with cystic fibrosis.149 Researchers report that a 22.2 ppb (interquartile range) 

increase in ozone concentration can lead to a 52 percent increase in the risk of respiratory 

exacerbation in children and adolescents with cystic fibrosis 48 hours after exposure, after 

controlling for other risk factors. Researchers indicated that the WHO Air Quality Guidelines, 

already more stringent that the NAAQS, should be lowered by at least 25 percent to minimize 

risks of pulmonary exacerbations in this high-risk population, concluding: 

The interaction between ozone and lung epithelial lining fluid in patients with CF most 

likely produces oxidized species that may be responsible for triggering lung inflammation 

 

145 R. Spencer-Hwang et al. (2011). Ambient air pollutants and risk of fatal coronary heart disease among kidney 

transplant recipients, Am. J. Kidney Dis., 58(4): 608-16.

146 Bhinder S, Chen H, Sato M, Copes R, Evans GJ, Chow CW, Singer LG. Air pollution and the development of 

post-transplant chronic lung allograft dysfunction. Am J Transplant 2014; 14 (12): 2749-57.

147 Cystic Fibrosis Foundation, About CF, available at http://www.cff.org/AboutCF (accessed Mar. 15, 2015).

148 Id.

149 S. Farhat, et al. (2014). Ozone is associated with an increased risk of respiratory exacerbations in patients with 

cystic fibrosis, Chest, 144(4): 1186-1192. 
45

and contribute to acute bronchoconstriction and airway hyperresponsiveness, similar to 

the changes observed in asthma.150

An editorial in the journal Chest reviewing study commented: 

These results show that ground-level ozone air pollution has substantial adverse effects 

on the respiratory health of patients with cystic fibrosis and that the current US 

Environmental Protection Agency standards are not sufficient to protect the respiratory 

health of these patients. 151

An earlier, much larger study of 11,484 cystic fibrosis patients aged 6 years and older, who lived 

within 30 miles of an air quality monitor, found that a 10 ppb rise in ozone was associated with 

increased risk of pulmonary exacerbations.152 Collectively these studies suggest that cystic 

fibrosis patients have been overlooked as a susceptible population. 

8. Due to the Risk of Reproductive and Developmental Effects, Pregnant 

Women Should Be Considered a Sensitive Group 

Pregnant women and their fetuses are another population that should be considered 

especially susceptible to air pollution. A number of recent studies have reported associations 

between exposure to air pollution and adverse pregnancy outcomes such as pre-eclampsia, 

preterm birth, and low birth weight babies. For example, a prospective register-based cohort 

study in Stockholm, Sweden observed an increased risk with ozone exposure in the first trimester 

for preterm birth and pre-eclampsia. Researchers estimated one in twenty cases of pre-eclampsia 

to be associated with ozone exposure.153 A study published in 2012 assessed the association 

between ambient pollutant concentrations and term birth weight for 1.5 million births in Texas 

from 1998 to 2004. Lower birth weight was associated with ozone exposure in the first and 

second trimester.154 Another study in North Carolina reported that ozone concentrations in both 

urban and rural areas may be associated with an increased risk of term low birth weight and 

small for gestational age births.155 

These are just a few of the studies look at air pollution concentrations and adverse

pregnancy outcomes and which strongly suggest that pregnant women are especially vulnerable 

to exposure to ozone pollution. To comply with its Clean Air Act mandate, EPA must set 

standards to protect pregnant women and their fetuses.

 

150 Id. 

151 H.J. Farber (2013). Public policy, air quality, and protecting the most vulnerable, Chest, 144(4): 1093-4.

152 Goss, et al. (2004). Effect of ambient air pollution on pulmonary exacerbations and lung function in cystic 

fibrosis, Am. J. Respir. Crit. Care Med., 169 (7): 816-21.

153 D. Olsson, I. Mogren, & B. Forsberg (2013). Air pollution exposure in early pregnancy and adverse pregnancy 

outcomes: a register-based cohort study, BMJ Open, 3(2).

154 L.A. Geer, J. Weedon, & M.L. Bell (2012). Ambient air pollution and term birth weight in Texas from 1998 to 

2004, J. Air Waste Manag. Assoc., 62 (11): 1285-95.

155 L.C. Vinikoor-Imler (2014). Associations between prenatal exposure to air pollution, small for gestational age, 

and term low birthweight in a state-wide birth cohort, Environ. Res., 132: 132-9.
46

D. Based on the Demonstrated Impacts to Healthy Individuals at 60 ppb, the 

Impacts to Sensitive Populations at 60 ppb Are Properly Characterized as 

Adverse

In making judgments as to when various ozone-related effects become regarded as 

adverse to the health of individuals, EPA has explained that it looks to guidelines published by 

the American Thoracic Society (ATS)156, as well as the advice of CASAC.157 Effects may be 

adverse at the individual or population level. For example, at the individual level, ATS guidance 

concludes that “transient, reversible loss of lung function in combination with respiratory 

symptoms should be considered adverse.”158 ATS has also identified as adverse “medically 

significant physiologic changes generally evidenced by” (among other things) “[i]nterference 

with the normal activity of the affected person or persons.”159 Additionally, effects may be 

adverse at the population level. As EPA explains, “[e]xposure to air pollution that increases the 

risk of an adverse effect to the entire population is adverse, even though it may not increase the 

risk of any individual to an unacceptable level.”160 Based on the ATS guidance and CASAC’s 

advice to EPA regarding the proper characterization of adverse impacts, it is clear that known 

impacts to sensitive populations at levels of 60 ppb are properly characterized as adverse. 

1. Children and Adults with Lung Disease Will Experience Impacts 

Properly Characterized as Adverse Based on Exposures to 60 ppb

While CASAC advised that “[e]stimation of FEV1 decrements of ≥15 percent is 

appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy 

adults,”161 CASAC also concluded that lung function decrement greater than 10 percent in 

sensitive populations including children and adults with lung disease would interfere with normal 

activity for many individuals and would likely result in additional and more frequent use of 

medication.162 As CASAC advised,

for children and adults with lung disease, even moderate functional (e.g., FEV1 

decrements ≥ 10 percent but < 20 percent, lasting up to 24 hours) or symptomatic 

responses (e.g., frequent spontaneous cough, marked discomfort on exercise or 

with deep breath, wheeze accompanied by shortness of breath, lasting up to 24 

hours) would likely interfere with normal activity for many individuals, and 

would likely result in additional and more frequent use of medication.

163

 

As ATS explains in its 2000 guidance on adverse effects, a change in medication 

constitutes a change in clinical status and an adverse health impact at the individual level: 

 

156 American Thoracic Society (2000). What Constitutes an Adverse Health Effect of Air Pollution? Am. J. Respir. 

Crit. Care Med., 161:665-673 [hereinafter ATS 2000].

157 Proposed Rule at 75,263. 

158 Proposed Rule at 75,263. 

159 Id. at 75263/1.

160 Id. at 75263.

161 Id., quoting CASAC Letter 2014a at 3.

162 Id. 

163 Id. at 75,263-4, citing U.S. EPA, 2007, p.3-72; 72 FR 37849, July 11, 2007.
47

The committee judged that air pollution-related symptoms associated with 

diminished quality of life or with a change in clinical status should be considered 

as adverse at the individual level. Characterizing the degree of symptomatology 

associated with diminished quality of life is an appropriate focus for research and 

a topic that could be investigated using new approaches for assessing quality of 

life. A change in clinical status can be appropriately set in a medical framework 

as one requiring medical care or a change in medication.

164

 

Recent controlled human exposure studies conducted with healthy adults show that 60 

ppb for 6.6 hours results in lung function decrement >10 percent for 10 percent of individuals.165

As discussed extensively in section IV.B.2.a above, children are more sensitive to ozone 

pollution than adults.166 Consequently, exposures of 60 ppb for 6.6 hours for children and for 

adults with lung disease are anticipated to result in additional and more frequent use of 

medication, a change in clinical status that ATS and CASAC consider to be adverse at the 

individual level. 

2. Individuals with Pre-existing Pulmonary or Cardiac Disease Will 

Experience Impacts Properly Characterized as Adverse Based on 

Exposures to 60 ppb

Similarly, CASAC advises that 10 percent decrements in FEV1 can lead to respiratory 

symptoms in individuals with pre-existing pulmonary or cardiac disease.167 These populations 

are at least as sensitive as healthy adults who were in the controlled human exposure studies.168

As ATS explained, “by definition, susceptible individuals cannot have the same margin of safety 

as the non-susceptible groups within the population.”169 ATS recommends, and EPA 

acknowledges, that a combination of lung functions decrements of 10 percent in FEV1 and 

respiratory symptoms is adverse.170 Consequently, it is clear that individuals with pre-existing 

pulmonary or cardiac disease are likely to experience impacts properly characterized as adverse 

based on exposures to 60 ppb.

 

164 American Thoracic Society. What constitutes an adverse health effect of air pollution? Official statement of the 

American Thoracic Society. Am J Respir Crit Care Med 2000; 161 (2 Pt 1): 665-73.

165 Proposed Rule at 75,250/2 & n.37 (noting that percentage is an underestimate).

166 See also Proposed Rule at 75,246 (“[A]t-risk populations or lifestages, such as people with asthma or children, 

are expected to be affected more by [exposures of concern] than healthy adults.”) EPA in a footnote in the proposed 

rule observes that the HREA’s estimates of lung function decrements are “based on the assumption that children 

exhibit the same lung function responses following O3 exposures as healthy 18 year olds,” citing a 30-year old study 

of 8-11 year old children. Id. at 75,248, n.28. Given the differing physiology of children discussed in section

IV.B.2.a, reliance on a single study involving 8- to 11-year old children to conclude they experience the same lung 

function decrements would be arbitrary. Nevertheless, even if reliance on the results of this study was rational, it 

would not diminish the conclusion that a substantial subset of children would experience lung function decrements 

of at least 10% when exposed to concentrations of 60 ppb for periods of 6.6 hours, as occurred in healthy adults. 

167 Proposed Rule at 75,264 (“In addition, in their letter advising the Administrator on the reconsideration of the 

2008 final decision, CASAC stated that ‘[a] 10% decrement in FEV1 can lead to respiratory symptoms, especially in 

individuals with pre-existing pulmonary or cardiac disease.’”). 

168 ATS 2000.

169 Id.

170 See ATS 2000 at 671 (“this committee recommended that reversible loss of lung function in combination with the 

presence of symptoms should be considered adverse.”).
48

3. Individuals with Asthma Will Experience Impacts Properly 

Characterized as Adverse Based on Exposures to 60 ppb

The same analysis as above applies to individuals with asthma. As EPA acknowledges, 

“[i]n this review, CASAC concurred that ‘[a]n FEV1 decrement of ≥10 percent is a scientifically 

relevant surrogate for adverse health outcomes for people with asthma and lung disease’.”171

Indeed, in the last ozone NAAQS review, EPA itself agreed that lung function decrements of 10 

percent in FEV1 standing alone were adverse for people with asthma.172 Moreover, asthmatics 

have been found to have double the decrements in lung function of healthy people when exposed 

to the same levels of ozone.173 Given that a statistically significant percentage of healthy adults 

were found to experience lung function FEV1 decrements of >10 percent when exposed to levels 

of 60 ppb for 6.6 hours, asthmatics and other individuals with lung disease would experience 

FEV1 decrements far in excess of 10 percent when similarly exposed to ozone concentrations of 

60 ppb for 6.6 hours. In light of CASAC’s advice that such lung function decrements are an 

“adverse health outcome” for these sensitive groups, it is clear that these groups would 

experience impacts properly characterized as adverse based on exposures to 60 ppb. 

4. Lung inflammation in Healthy Adults at 60 ppb is Properly 

Characterized as Adverse

In its proposal, EPA observes that “[e]vidence new to this review indicates that 6.6-hour 

exposures to 60 ppb O3 during moderate exertion can result in pulmonary inflammation in 

healthy adults (based on study mean).”174 EPA explains that: 

As discussed in the ISA, the initiation of inflammation can be considered as 

evidence that injury has occurred. Inflammation induced by a single O3 exposure 

can resolve entirely but, as noted in the ISA (U.S. EPA, 2013a, p. 6-76), 

‘continued acute inflammation can evolve into a chronic inflammatory state,’ 

which would be adverse.175

“Unlike O3-induced decrements in lung function, which are attenuated following repeated 

exposures over several days . . . some markers of O3-induced inflammation and tissue damage 

remain elevated during repeated exposures, indicating ongoing damage to the respiratory 

system.”176 Because this continued acute inflammation can evolve into a chronic inflammatory 

state, which EPA acknowledges to be adverse, the evidence of pulmonary inflammation when 

healthy adults are exposed to ozone at concentrations of 60 ppb for 6.6 hours must be considered 

adverse. 

 

171 Proposed Rule at 75,264, citing CASAC Letter 2014a. 

172 73 Fed. Reg. at 16,454/3-55/1 (Mar. 27, 2008).

173 Proposed Rule at75,265 (“For instance, Horstman et al. (1995) observed that mild-to-moderate asthmatics, on 

average, experienced double the O3-induced FEV1 decrement of healthy subjects (19% versus 10%, respectively, p 

= 0.04).”). 

174 Id. 75,264. 

175 Id. 75,264; see also Policy Assessment at 3-19 (“In addition, one recent controlled human exposure study has 

reported O3-induced PMN influx following exposures of healthy adults to O3 concentrations of 60 ppb (Kim et al., 

2011), the lowest concentration at which inflammatory responses have been evaluated in human studies.”). 

176 Policy Assessment at 3-19, citing U.S. EPA, 2013, section 6.2.1.1 and 6.2.3.1, p. 6-81.
49

5. Population Level Effects Linked to Ozone Exposures at Levels of 60 

ppb are Properly Characterized as Adverse. 

In its guidance on adverse impacts, ATS makes clear that “[a]t the population level, any 

detectable increment in symptom frequency should be considered as constituting an adverse

health effect.”177 Noting that “[a] wide range of clinical outcome measures has been considered 

in relation to air pollution, including population-level effects, such as increases in numbers of 

emergency room visits for asthma or hospitalizations for pneumonia, and individual level effects, 

such as increased need for bronchodilator therapy,” ATS explained that: “The present committee 

shared the view of the previous group: detectable effects of air pollution on clinical measures 

should be considered adverse.”

178

A robust epidemiological literature links exposure to ozone at levels of 60 ppb with 

numerous clinical measures. As discussed in section V.B below, many studies have 

demonstrated an independent association of short-term exposures of ozone to premature

mortality, and respiratory and cardiac effects, often at mean or median concentrations of 60 ppb 

and below. In addition, epidemiological studies support the ISA’s conclusion that there is a 

likely causal relationship between long-term exposures to ozone and respiratory effects. 

Moreover, the ISA finds that “long term ozone exposure is associated with adverse effects 

ranging from episodic respiratory illness to permanent respiratory injury to progressive 

respiratory decline.”179 The ISA document details numerous studies showing that long-term 

exposures to ozone are associated with new onset asthma, increased asthma symptoms, increased 

risk of asthma hospital admissions, deficits in lung function growth rate in children, and 

increased risk of premature death. These population level “detectable effects of air pollution on 

clinical measures” occurring at levels of 60 ppb are properly considered adverse. 

Further, as discussed more fully below, the statistically significant group mean decrease 

in FEV1 observed in controlled human exposure studies as low as 60 ppb is an adverse effect at 

the population level. In the last revision of the sulfur dioxide (“SO2”) NAAQS, EPA correctly 

found that “diminished reserve lung function in a population that is attributable to air pollution is 

considered an adverse effect under ATS guidance.”180 Decrements of that type occur in 

controlled human exposure studies at ozone levels down to 60 ppb.

V. COMMENTS ON THE PROPOSAL

A. The Current Standard of 75 ppb Does Not Protect the Public Health with an 

Adequate Margin of Safety As Required by the Clean Air Act

EPA correctly acknowledges adverse health effects caused by ozone levels of 75 ppb and 

the need to revise the primary standard in order to protect public health. Based on current 

scientific evidence, risk assessment modeling, CASAC advice, and public comment, EPA 

 

177 ATS 2000 at 671 (emphasis added). 

178 Id. (emphasis added).

179 ISA Section 7.2.8 

180 75 Fed. Reg. 35,220, 35,226/2 (June 22, 2010).
50

concludes that the current primary standard of 75 ppb “is not requisite to protect public health 

with an adequate margin of safety, and that it should be revised to provide increased public 

health protection.”181 

The fact that the current primary standard of 75 ppb is inadequate to protect public health 

and meet the requirements of the Clean Air Act is not new, however, and has long been 

recognized by EPA and its scientific advisors. According to EPA, “significant risks to public 

health are likely to occur at a standard level of 0.075 ppm,” which is “not sufficient to meet the 

statutory requirement that the standard be set at a level requisite to protect public health with an 

adequate margin of safety.”182

As discussed below, CASAC has also repeatedly and unanimously advised EPA that the 

current primary standard of 75 ppb is not protective of human health and recommended a more 

protective standard including after the standard was set, during the reconsideration, and in this 

current review.183

The scientific record before EPA today is inarguably stronger than in prior reviews, 

including those concluding in 2008 and 2011. EPA has determined that revising the primary 

standard is warranted to protect against adverse health effects that include decreased lung 

function and respiratory symptoms, serious morbidity, and premature mortality.184 Since the last 

scientific review, evidence of health impacts caused by exposure to ozone pollution has 

strengthened significantly. The record shows extensive evidence that the present 75 ppb

standard allows adverse health effects for millions of Americans each year, including early 

death, hospitalization, and asthma attacks. As described in the previous sections, controlled 

human exposure studies demonstrate adverse health impacts at levels below the current standard. 

In healthy adults and at exposures of only 6.6 hours, lung function decrements and respiratory 

symptoms are seen that clearly meet the ATS criteria for an adverse response.

Further, EPA has demonstrated the critical public health impacts experienced by 

concentrations at the current standard. According to the HREA’s modeling, when meeting the 

current primary standard, 3-8 percent of children in the 15 urban study areas examined - or 

900,000 children, including 90,000 children with asthma - would experience repeated exposures 

of concern to ozone concentrations higher than 60 ppb.185 In years with especially poor air 

quality, over 14 percent of children would be expected to experience repeat exposures to ambient 

ozone concentrations above 60 ppb. Under the current standard, the HREA’s numbers for single 

exposure incidents are even higher: 10-17 percent of children in the 15 urban areas would 

 

181 Proposed Rule at 75,236.

182 Letter from U.S. EPA Administrator Lisa P. Jackson to the Honorable James Inhofe, May13, 2011. (See Exhibit 

1).

183 Letter from CASAC Chair Dr. Rogene Henderson to U.S. EPA Administrator Stephen L. Johnson on CASAC 

Recommendations Concerning the Final Rule for the National Ambient Air Quality Standards for Ozone (EPACASAC-08-009), Apr. 7, 2008 (See Exhibit 2); Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA 

Administrator Lisa P. Jackson on CASAC Response to Charge Questions on the Reconsideration of the 2008 Ozone 

National Ambient Air Quality Standards, (EPA-CASAC-11-004), Mar. 30, 2011 (See Exhibit 3); CASAC Letter 

2014a. 

184 Policy Assessment at 3-1, 135-136.

185 Id. at 3-100; HREA chapter 5. 
51

experience (one or more) exposures to concentrations higher than 60 ppb - corresponding to 

almost 2.5 million children of whom 250,000 are asthmatics - and up to 26 percent of children in 

bad years.186 The HREA predicts that if the current standard were met, 14 to 19 percent of 

children would experience lung function decrements, corresponding to approximately 3 million 

children (in the case study areas alone), of whom about 300,000 have asthma.

187 Nationally, far 

more children experience exposures of concern and lung function decrements. Thousands are 

estimated to die each year based upon exposure to ozone when complying with a primary 

standard of 75 ppb.188

Overwhelming evidence documents that the current standard fails to protect public 

health. EPA is correct, although too conservative, in concluding that the “the available evidence 

and exposure and risk information clearly calls into question the adequacy of public health 

protection provided by the current primary standard.”189

1. Broad Scientific Consensus Supports a More Protective Standard

Than 75 ppb

a. Since 2008 CASAC Has Consistently Supported Lowering the 

Standard Below 75 ppb

The Clean Air Act assigns responsibility for reviewing the air quality criteria and making 

recommendations on revisions of the NAAQS to the Clean Air Scientific Advisory Committee 

(CASAC). CASAC is an independent review committee comprised of leading scientific experts 

from universities, state government, and industry. Members of the committee have expertise in 

diverse scientific disciplines ranging from atmospheric science, toxicology, dosimetry, 

biostatistics, pulmonary medicine, epidemiology, ecology, risk assessment, monitoring, and 

other fields relevant to the review of the NAAQS. There are seven members of the statutory 

CASAC and additional consulting members are impaneled for each review to ensure that the 

committee has appropriate expertise in all pertinent disciplines. CASAC has an extensive record 

of providing independent peer review of EPA documents related to the ozone NAAQS. 

Three separate CASAC committees, under three different Chairs, have unanimously 

confirmed that the current ozone standard is not protective of public health and that the standard 

should be set in the range of 60 to 70 ppb. Indeed, as noted below, CASAC has concluded that 

the standard should be set at the lower end of this range. 

The first such committee was convened for the review that culminated in the 2008 

revisions to the standard. From 2005 to 2008, CASAC reviewed two drafts of the Staff Paper, 

two drafts of the Criteria Document, two drafts of the risk assessment and two drafts of the 

exposure assessment. The Committee wrote to EPA Administrator Stephen L. Johnson three 

times, on October 24, 2006, March 26, 2007 and April 7, 2008, unanimously recommending 

selection of an 8-hour average ozone NAAQS within the range of 60 to 70 ppb and (Henderson, 

 

186 Id.

187 Policy Assessment at 3-111; HREA chapter 6.

188 Id.

189 Policy Assessment at ES-3, 3-1.
52

taking the unusual step of commenting on the final rule (published Mar. 12, 2008) to register its

concern that 75 ppb was not protective of public health.190 

The second committee was constituted during the administrative reconsideration process 

following the 2008 review. In response to EPA’s reconsideration of the 2008 ozone NAAQS and 

the proposal published on January 19, 2010, CASAC reaffirmed its support for the selection of 

an 8-hour average ozone NAAQS within the 60–70 ppb range.191

During the reconsideration process, EPA requested specific advice from CASAC on a 

number of important scientific questions under consideration. The Committee responded to these 

charges in an extremely detailed letter.192 The letter again reaffirmed the Committee’s scientific 

judgment that:

the evidence from controlled human and epidemiological studies strongly 

supports the selection of a new primary ozone standard within the 60–70 ppb 

range for an 8-hour averaging time. As enumerated in the 2006 Criteria Document 

and other companion assessments, the evidence provides firm and sufficiently 

certain support for this recommended range for the standard.193

The second CASAC also reached a number of other specific findings and provided supporting 

evidence that is relevant to the current review:194

 Healthy individuals have been shown to have clinically relevant responses, even at 60 

ppb. 

 Since the majority of clinical studies involve young, healthy adult populations, less is 

known about health effects in such potentially ozone sensitive populations as the elderly, 

children and those with cardiopulmonary disease. For these susceptible groups, 

decrements in lung function may be greater than in healthy volunteers and are likely to 

have a greater clinical significance. 

 Children and adults with asthma are at increased risk of acute exacerbations on or shortly 

after days when elevated ozone concentrations occur, even when exposures do not exceed 

the NAAQS concentration of 75 ppb. 

 Large segments of the population fall into what EPA terms a “sensitive population 

group,” i.e., those at increased risk because they are more intrinsically susceptible 

 

190 Letter from CASAC Chair Dr. Rogene Henderson to U.S. EPA Administrator Stephen L. Johnson on CASAC’s 

Peer Review of the Agency’s Final Ozone Staff Paper (EPA-CASAC-07-001), Oct. 24, 2006; Letter from CASAC 

Chair Dr. Rogene Henderson to U.S. EPA Administrator Stephen L. Johnson on CASAC’s Review of the Agency’s 

2

nd Draft Ozone Staff Paper (EPA-CASAC-07-002), Mar. 26, 2007; Letter from CASAC Chair Dr. Rogene 

Henderson to U.S. EPA Administrator Stephen L. Johnson on CASAC Recommendations Concerning the Final 

Rule for the National Ambient Air Quality Standards for Ozone (EPA-CASAC-08-009), Apr. 7, 2008.

191 Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA Administrator Lisa P. Jackson on Review of 

EPA’s Proposed Ozone National Ambient Air Quality Standard (Federal Register, Vol. 75, Nov. 11, Jan. 19, 2010) , 

(EPA-CASAC-10-007), Feb. 9, 2010. 

192 Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA Administrator Lisa P. Jackson on CASAC 

Response to Charge Questions on the Reconsideration of the 2008 Ozone National Ambient Air Quality Standards, 

(EPA-CASAC-11-004), Mar. 30, 2011. 

193 Id.

194 Id.
53

(children, the elderly, and individuals with chronic lung disease) and those who are more 

vulnerable due to increased exposure because they work outside or live in areas that are 

more polluted than the mean levels in their communities.

These comments were based solely on the science record available for the 2008 review, 

for which the scientific record closed in 2006. The letter provides the Committee’s consensus 

scientific advice regarding such important issues – such as the adversity of effects, the responses 

of sensitive populations, and other matters that will be discussed in more detail below.195

b. CASAC Concluded That a 70 ppb Standard Provides “Little” 

Margin of Safety and Specifically Cited a Level of 60 ppb as 

Meeting the Requirements to Protect Public Health. 

The current CASAC committee has agreed with the previous two panels about the underprotectiveness of the current 75 ppb standard, and now underlined the limitations at the top end 

of a 60 to 70 ppb range. This panel included certain members who had served on the two 

previous panels, but also new members who had not previously served. All told, 44 individuals 

served on one or more CASAC ozone review panels. It is remarkable that 44 scientists from 

universities across the country and a range of expertise all reached a unanimous conclusion that 

the current standard fails to protect public health and that the 8-hour NAAQS must be revised 

downward to protect public health. 

As discussed above in Section II.G., the Administrator is bound by the Clean Air Act to 

give due deference to the advice of CASAC. In light of this legal requirement, it is particularly 

indefensible that the proposal departs from the CASAC consensus recommendations by 

eliminating the more health-protective 60 ppb option specifically recommended by CASAC, 

especially in light of CASAC’s finding that 60 ppb is a scientifically justifiable lower bound 

based on findings of adverse effects at that level. 196

In its most recent letters to the EPA Administrator concerning the current review, the 

CASAC panel made clear that there is “sound” and “clear” scientific support to strengthen the 

standard to the lower end of a range between 60 and 70 ppb. Summarized below and discussed 

in more detail following, CASAC reached these conclusions about the range then under 

consideration:

 The current standard is inadequate to protect public health,

 At 70 ppb, there is substantial scientific evidence of adverse effects, including decrease in 

lung function, increase in respiratory symptoms, and increase in airway inflammation,

 

195

 Indeed, CASAC’s conclusions that the current standard of 75 ppb is insufficient is consistent with EPA’s own 

staff scientists’ Policy Assessment “...available health evidence and exposure/risk information calls into question 

the adequacy of the public health protection provided by the current standard,” Policy Assessment at 4-73, and that 

EPA should be considering a “range of 70 ppb to 60 ppb.” Id. 4-75. In its review of the second draft Policy 

Assessment, CASAC took issue with EPA’s staff recommendations, in advising that the upper end of the range be 

below 70 ppb.

196 CASAC Letter 2014a at 7.
54

 The standard should be set below 70 ppb to meet the statutory requirement in the Clean 

Air Act to protect public health with an adequate margin of safety, and

CASAC has made expressly made clear that it views the higher end of the range that EPA 

proposes as insufficient to prevent adverse effects:

At 70 ppb, there is substantial scientific evidence of adverse effects . . . including 

decrease in lung function, increase in respiratory symptoms, and increase in airway 

inflammation. Although a level of 70 ppb is more protective of public health than the 

current standard, it may not meet the statutory requirement to protect public health with 

an adequate margin of safety.

Thus, our policy advice is to set the level of the standard lower than 70 ppb within a 

range down to 60 ppb, taking into account your judgment regarding the desired margin of 

safety to protect public health, and taking into account that lower levels will provide 

incrementally greater margins of safety.197

CASAC’s advice in 2014 is considerably stronger and more explicit than CASAC’s 

advice during the 2008 review and the reconsideration in 2011. Both previous reviews were 

based on a record of evidence that ended in 2006. However, the 2014 review is based on the 

overwhelming scientific and medical evidence of ozone’s adverse health impacts--even at 70 

ppb--that has amassed since 2006. And it is overwhelming. With more than 1,000 new studies 

included in the current review, the newer evidence documented the weaknesses of any potential 

standard above 60 ppb. 

For example, in its letter to EPA, CASAC specifically found that the choice of 60 ppb as 

the lower end of the recommended range was justified scientifically “based on findings of 

adverse effects, including clinically significant lung function decrements and airway 

inflammation, after exposures to 60 ppb ozone in healthy adults with moderate exertion.”

198

 

CASAC further emphasizes that these findings likely understate adverse impacts in sensitive 

populations. For example, children with asthma are likely to experience more significant 

adverse effects at 60 ppb than demonstrated in healthy adults: “[The] clinical studies do not 

address sensitive subgroups, such as children with asthma, and that there is a scientific basis to 

anticipate that the adverse effects for such subgroups are likely to be more significant at 60 ppb 

than for healthy adults.”

199

 

In writing to EPA, CASAC could not be clearer that exposures to 70 ppb ozone are of 

significant concern for children, asthmatics, the elderly and other susceptible populations. 

[A] level of 70 ppb offers only modest incremental reductions in short-term mortality risk 

compared to the current standard. Taken as a whole, these findings indicate that ozone 

exposures of 70 ppb pose reduced risk compared to the current standard but, nonetheless, 

are of significant concern, especially for children, asthmatics, the elderly and other at risk 

 

197 Id.

198 Id.

199 Id.
55

populations.200

The studies in the record, including the studies cited at length by CASAC to EPA, inform 

our understanding of the health impacts of ozone at low concentrations. As discussed in greater 

detail below, the ISA reaches stronger conclusions about the causality for a broad range of health 

endpoints, there is new evidence of adverse effects at low concentrations and there is new 

information on the extent of populations at risk since the last review. All of these factors 

informed CASAC’s decision to find that adverse effects occur at 70 ppb, to recommend a range 

below 70 ppb, and to conclude that 60 ppb should be the lower end of the range considered based 

on findings of adverse effects at that level.

Given CASAC’s clear recommendations, it is arbitrary and unlawful that EPA’s Draft 

Rule proposes a range that essentially dismisses much of the evidence since 2006, as well as 

CASAC’s assessment of the evidence. EPA’s inclusion of 70 ppb in its proposed range when 

CASAC specifically found substantial scientific certainty of adverse effects at that level and that 

standard should be set below 70 ppb, runs counter to the evidence in the record and to EPA’s 

own independent scientific advisors. And it is arbitrary and unlawful that EPA’s proposed range 

fails to include the more health-protective half of the range recommended by CASAC, including 

the level of 60 ppb at which CASAC determined that adverse effects had been found. Indeed, 

where, as here, the evidence has strengthened since 2006, it is arbitrary for EPA to propose a less 

protective range than the 60-70 ppb range it proposed in the 2010 reconsideration rule that was 

based solely on that older evidence. Simply put, EPA’s actions cannot be justified on the record 

before it, particularly why it has veered from years of unanimous recommendations by CASAC 

to include 60 ppb in the range under consideration. 

c. The Children’s Health Protection Advisory Committee 

Recommends a Standard of 60 ppb

EPA’s own Children’s Health Protection Advisory Committee (CHPAC) has been clear 

that the level of the NAAQS requisite to protect children’s health is 60 ppb. The Committee is 

charged with advising the EPA regarding regulatory actions, research and communications 

related to children’s health. The Committee is comprised of 24 experts on children’s health from 

academia, state government, and the research community. CHPAC has repeatedly recommended 

that EPA revise the ozone NAAQS to 60 ppb. Most recently in 2014, the Committee stated: 

Children suffer a disproportionate burden of ozone-related health impacts due to critical 

developmental periods of lung growth in childhood and adolescence that can result in 

permanent disability. In addition, children have increased susceptibility due to increased 

ventilatory rates and increased outdoor physical activity compared with adults. The 6.8 

million children suffering from asthma in the US are some of the most vulnerable to 

ozone-related respiratory impacts.

201

 

200 Id.

201 Letter from CHPAC Chair Dr.Sheela Sathyanarayana to CASAC Chair Dr. Christopher Frey, May 19, 2014. (See 

Exhibit 4). 
56

Because of the children’s developmental stage and increased exposure to ozone, and in light of 

expanding evidence of adverse health effects in children, CHPAC recommended an 8-hour 

average ozone standard of 60 ppb: 

In 2007, the US EPA Children’s Health Protection Advisory Committee (CHPAC) 

submitted two letters to Administrator Johnson that highlighted scientific findings 

regarding ozone-related children’s health effects and urged [EPA] to support an ozone 

standard of 60 ppb in order to adequately protect children’s health with a sufficient 

margin of safety. I am writing now to strongly re-affirm the recommendation of 60 ppb 

based on the expanding scientific evidence base documenting adverse childhood health 

impacts in relation to ambient ozone exposure. The higher end of the range, 60 ppb – 70 

ppb, put forth by the Clean Air Scientific Advisory Committee (CASAC) in 2007 will not 

be sufficient to protect children’s health.202

d. Medical and Public Health Organizations Support a Standard 

of 60 ppb

There is broad consensus in the medical community that the NAAQS must be revised to a 

level of 60 ppb to protect public health from harmful ambient ozone pollution.

On August 3, 2011, fourteen leading medical and public health organizations cosigned a letter to 

the President203 stating the following: 

The ozone health standard must protect those who are most vulnerable from the 

dangerous health impacts of ozone, including infants, children, older adults, and those

with chronic diseases. To safeguard the health of the American people, help to save lives, 

and reduce health care spending, we support the most protective standard under 

consideration: 60 parts per billion (ppb) averaged over eight hours. 

Signers of the letter included American Academy of Pediatrics, American Association of 

Cardiovascular and Pulmonary Rehabilitation, American College of Preventive Medicine, 

American Heart Association, American Lung Association, American Public Health Association, 

American Thoracic Society, Asthma and Allergy Foundation of America, National Association 

for Medical Direction of Respiratory Care, National Association of County and City Health 

Officials, National Environmental Health Association, National Home Oxygen Patients 

Association, Physicians for Social Responsibility, and Trust for America's Health.

 

The American Thoracic Society (ATS), the leading medical association dedicated to 

advancing the clinical and scientific understanding of pulmonary diseases, speaks with authority 

on the adverse impacts of air pollution on health. ATS offered qualified applause to EPA’s 

proposal, stating: 

 

202 Id.

203 Letter from medical and public health organizations to President Obama, Aug. 3, 2011, available at 

http://c.ymcdn.com/sites/www.acpm.org/resource/resmgr/policy-files/2011_ltr_presidentozone.pdf. (See Exhibit 5).

203 ATS, Press Release: ATS Applauds EPA’s Proposed National Ambient Air Quality Standard for Ozone, Nov. 26, 

2014, available athttp://www.thoracic.org/newsroom/press-releases/journal/articles/ats-applauds-epas-proposednational-ambient-air-quality-standard-for-ozone.php.
57

The ATS has long supported an 8-hour ozone standard of 0.060 parts per million (ppm)

to best protect public health.

Recent evidence links ozone pollution and adverse health effects including studies 

showing dose-response relationships between ozone exposure and hospital admissions for 

asthma in children and hospital admissions for asthma and COPD in adults, lung function 

deficits in healthy adults exposed to ozone at levels between 0.060 and 0.070 ppm, and an 

increased mortality risk associated with ozone exposure, primarily affecting the elderly 

and patients with chronic diseases. 204 T

The American Thoracic Society discussed its position further in an editorial in the American 

Journal of Respiratory and Critical Care Medicine.

205

 8-hour 

In 2007, 2010, and now again in 2014, the American Thoracic Society (ATS) has 

recommended that the U.S. Environmental Protection Agency (EPA) adopt an 8-hour 

ozone national ambient air quality standard of 60 ppb in order to adequately protect 

public health(1, 2). While the recommended standard endorsed by ATS has not changed 

during this time, the scientific evidence supporting this recommendation has significantly 

strengthened . . . .

Highlights of this new body of evidence include a study of emergency department visits 

among children aged 0 to 4 in Atlanta, which found that each 30 ppb increase in the 3-

day average of ozone was associated with an 8 percent higher risk of pneumonia and a 4

percent higher risk for upper respiratory infection(5) [Darrow et al 2014]. Several studies 

have demonstrated dose-response relationships between ozone exposure and childhood 

asthma admissions at exposure levels in the 60 to 80 ppb range (6–9) [Strickland et al 

2014, Strickland et al 2010, Gleason et al 2014, Silverman et al 2010]. Similar 

associations have been found for adult admissions for asthma (9–11) [Silverman and Ito 

2010, Glad et al 2012, Meg et al 2010] and COPD(12, 13) [Ko and Hui 2012, MediaRamon et al 20076]. A population-based cohort study of generally healthy adults found 

that FEV1 was 56 mL lower after days when ambient ozone ranged from 59 to 75 ppb 

compared to days with levels under 59 ppb(14) [Rice et al 2013]. Controlled human 

exposure studies have re-affirmed lung function decrements in healthy adults after 

exposure to 60 to 70 ppb of ozone(15,16) [Schelegle et al 2009, Kim et al 2011]. Perhaps 

of greatest concern, there is now stronger evidence of increased mortality in association 

with ozone (17–19)[Peng et al 2013, Romieu et al 2012,Zanobetti and Schwartz 2008], 

particularly among the elderly and those with chronic disease(20, 21)[Medina-Ramon 

and Schwartz 2008, Zanobetti and Schwartz 2011]”.

Likewise, the American Academy of Pediatrics has also endorsed a standard of 60 ppb:

 

204 ATS, Press Release: ATS Applauds EPA’s Proposed National Ambient Air Quality Standard for Ozone, Nov. 26, 

2014, available athttp://www.thoracic.org/newsroom/press-releases/journal/articles/ats-applauds-epas-proposednational-ambient-air-quality-standard-for-ozone.php.

205 M.B. Rice, T.L. Guidotti, & K.R. Cromar (2014). on behalf of the ATS Environmental Health Policy Committee. 

Scientific Evidence Supports Stronger Limits on Ozone, Am. J. Crit. Care Med..
58

Scientific evidence strongly supports a level of 60 parts per billion . . . . Ozone pollution 

in the air disproportionately impacts children . . . whose unique health and developmental 

needs make them more susceptible to pollutants. 206 

And the American Medical Association, the nation’s largest medical society has also gone on 

record in support of a 60 ppb ozone standard in letters during the comment periods in both the

previous review and the reconsideration. 

207

e. Many Other Countries, and the World Health Organization, 

Have Concluded That a Standard of 75 ppb Is Far Too Weak 

and that the 65 – 70 ppb Range is Insufficient to Protect Public 

Health.

i. World Health Organization 

In October 2006, the World Health Organization (WHO) revised their international air 

quality guidelines for ozone.208 The prior guideline for 8-hour average ozone concentrations of 

120 μg/m3 (0.061 ppm) was reduced to 100 μg/m3 (0.051 ppm). The previous guideline and the 

new guideline are both substantially lower than both the current and proposed U.S. air quality 

standard. WHO provided a twofold basis for the revised guidelines. First, new epidemiological 

studies showed convincing evidence of associations between daily mortality and ozone levels.

Similar associations have been observed in both North America and Europe. These time-series 

studies have shown effects without clear evidence of a threshold. Second, evidence from both 

chamber and field studies also indicated that there is considerable individual variation in 

response to ozone. According to WHO, the previously recommended guideline value, “which 

was fixed at 120 μg/m3 8-hour mean [61 ppb], has been reduced to 100 μg/m3 [51 ppb] based on 

recent conclusive associations between daily mortality and ozone levels occurring at ozone 

concentrations below 120 μg/m3.”209

Likewise, Environment Canada and Health Canada adopted new ambient air quality 

standards for ozone in 2013 that are significantly more stringent than the range EPA is proposing 

in this process. The Canadian Ambient Air Quality Standard for ozone was lowered from the 8-

hour standard of 65 ppb down to 63 ppb, to take effect in 2015, and to 62 ppb to take effect in 

2020.

210

 

 

206 James M. Perrin, MD, FAAP, President of the American Academy of Pediatrics, AAP Statement on New Ozone 

Standards Proposal, Nov. 26, 2014.

207 Letter from American Thoracic Society, American Medical Association, et al. to U.S. EPA Administrator Lisa P. 

Jackson, Mar. 22, 2010. 

208 World Health Organization, WHO Air quality guidelines for particulate matter, ozone, nitrogen dioxide and 

sulfur dioxide. Global update 2005. Summary of risk assessment, available at

http://www.who.int/phe/air/aqg2006execsum.pdf

209 WHO, Ambient (outdoor) air quality http://www.who.int/mediacentre/factsheets/fs313/en/index.html

210 Environment Canada, Backgrounder: Canadian Ambient Air Quality Standards, available at

http://www.ec.gc.ca/default.asp?lang=En&n=56D4043B-1&news=A4B2C28A-2DFB-4BF4-8777-

ADF29B4360BD (accessed Mar. 16, 2015).
59

Once a leader in environmental protection, the United States now lags behind other 

developed and developing nations in the protectiveness of air quality standards for ozone. As 

shown in Table 3 that follows, numerous developed and developing countries have promulgated 

ozone standards that are more stringent than the current U.S. standard, and that are significantly 

more stringent than even the 65-70 ppb standard that EPA is proposing.

Table 3: Comparison of Ozone Standards Worldwide (ppb)211

 Country 1 hour 8 hour Exceedances 

Allowed per year

WHO 51

European Union -2010 61 25 (per 3 years)

Australia 100 80 (4-hr) 1

Cambodia 102

Canada 65 3

 (Jakarta) 102

Ireland 61

Japan 60

Malaysia 102 61

Mexico 110 1

Mongolia 61

New Zealand 76 0

People’s Republic of China (PRC) 

residential zone

61

PRC commercial zone 82

PRC industrial zone 102

Republic of Korea 102 61

Sri Lanka 102

Switzerland 61 1

Thailand 102 71

Viet Nam 92 61

United Kingdom 51 10

United States 75 3

B. EPA’s Proposal of 65-70 Fails to Protect the Public: EPA Must Revise the 

Primary NAAQS to a Level No Higher than 60 ppb

1. The Body of Science Evidence Demonstrates a Compelling Likelihood 

of Adverse Effects to Sensitive Populations at 60 ppb

As discussed at length above, there is overwhelming consensus among EPA’s advisors, 

independent medical and public health organizations, and regulatory bodies in other countries 

that the current standard of 75 ppb is insufficiently protective of the public health, that the high 

 

211 Compiled from online sources, including: Clean Air Initiative, Clean Air Initiative for Cities Around the World, 

available at http://www.cleanairnet.org/caiasia/1412/articles-71889_Ozone_standards.pdf; UK-AIR, Air 

Information Resource; available at www.airquality.co.uk/archive/standards.php; Ireland EPA, Air Quality 

Standards, available at http://www.epa.ie/air/quality/standards/#.VQcN_2MhArg; Aarhus University Department of 

Environmental Science, Air Quality Standards: (limit values, target values, etc.) available at 

http://www2.dmu.dk/AtmosphericEnvironment/Expost/database/docs/AQ_limit_values.pdf.
60

end of EPA’s proposed range under consideration—70 ppb—is insufficiently protective of 

public health, and that a lower level of 60 ppb is necessary to protect public health with an 

adequate margin of safety. As the following review of the primary scientific and medical 

research demonstrates, this consensus that 60 ppb is needed is well supported by the evidence in 

the record before EPA. 

a. As the ISA Reflects, the Scientific Record is Significantly 

Stronger in this Review than Prior Reviews and Warrants a 

Standard of 60 ppb

In this review, the scientific evidence laid out in the ISA is more robust and compelling 

across the board than what was available during the review completed in 2008 and the 

reconsideration. Using an objective, transparent, and vetted set of criteria, the ISA characterizes 

the strength of evidence for various health endpoints. Compared to the 2008 review, the causal 

findings are strengthened from “suggestive” to “likely causal” for cardiovascular effects and total 

mortality from short-term exposures, and for respiratory effects from long-term exposures. 

Furthermore, the evidence for central nervous system effects from short-term exposure and for 

cardiovascular effects, reproductive and developmental effects, central nervous system effects, 

and total mortality from long-term exposure strengthened to “suggestive of a causal 

relationship.” This stronger evidence necessitates greater public health protection. 

Based upon the substantial new information available, the 2013 ISA reached much 

stronger conclusions about the health effects of ozone than had been reached in the prior review 

of the science nine years earlier. The criteria for evaluating studies and reaching causal 

determinations is carefully laid out in the ISA, and has been thoroughly vetted by CASAC. 

Conclusions are reached based on multiple lines of evidence and multiple studies, demonstrating 

coherence, consistency, and plausibility. 

Specifically, the 2013 ISA reaches or identifies: 

 A conclusive determination that ozone causes adverse respiratory effects; 

 Several additional controlled human exposure studies demonstrating respiratory deficits 

and inflammation in healthy young adults at 60 ppb; 

 Stronger findings that the adverse effect of ozone on cardiovascular health are likely 

causal; 

 New information suggesting reproductive effects, such as increased risk of low birth 

weight babies; 

 New information about suggestive central nervous system and neurological effects; 

 New community health studies strengthening the link between ozone exposure and 

mortality, including at concentrations below the current standards; and 

 New information about the impact of longer-term exposures on respiratory health 

endpoints such as pulmonary inflammation and injury, and new onset asthma. 

Like the 2006 Air Quality Criteria Document, the 2013 ISA found there was a causal 

relationship between short-term exposure to ozone and respiratory effects. For almost every 

other health outcome and exposure duration evaluated, the ISA reached stronger causal 
61

determinations in 2013 than in 2008. For three critical health outcomes, scientific evidence in 

2013 was so strong enough to indicate a “likely causal relationship:” 

 Cardiovascular effects from short-term exposures; 

 Total mortality from short-term exposures; and 

 Respiratory effects from long-term exposures. 

ISA Table 1-1, below, compares the causal findings from the 2013 ISA with those of the 

2006 Criteria Document and highlights those health outcomes for which the causal 

determination has been strengthened since the last review.212

Table 4. ISA Table 1-1 on summary of ozone causal determinations

 

212 ISA at 2-23. 
62

Several other types of health effects are newly classified as suggestive of a causal relationship, 

by the 2013 ISA: 

 Central nervous system effects from short-term exposures; 

 Cardiovascular effects from long-term exposures; 

 Neurological effects from long-term exposure; and 

 Total mortality from long-term exposure. 

These stronger causal determinations are a reflection of the strength of evidence given 

scientific advancements since the last review, and refute EPA claims that uncertainty justifies 

rejection of standards lower than 65 ppb or supports selection of levels at or near 70 ppb.

The level of the standard must be based on consideration of these stronger causal 

findings. The new evidence indicates that a standard of 60 ppb is needed to protect public 

health. The evidence base for ozone is stronger than for any other air pollutant. There are strong 

lines of evidence from all three major scientific disciplines: toxicology, epidemiology, and 

controlled human exposure studies. Under the Clean Air Act, EPA is obliged to set air quality 

standards that protect public health from proven, as well as anticipated health effects. Revisions 

to the standards must reflect the increased strength of the evidence, and the breadth of adverse 

health effects now attributable to ozone air pollution. 

b. Controlled Studies Demonstrate Lung Function Decrements 

and Airway Inflammation at 60 ppb in Healthy Adults

As noted above, there are twice as many controlled human exposure studies available in 

this review. These studies show lung function decrements at 60 ppb in healthy young adults, 

including a new study indicating inflammation at 60 ppb. Again, inflammation is clearly an 

adverse effect, especially in asthmatics, and a ten percent decline in lung function, which was 

observed, is adverse for people with respiratory conditions whose breathing is already impaired. 

A primary standard below 60 ppb is needed to protect children, the elderly, and people with 

asthma. 

Strong evidence of the adverse effects of ozone pollution comes from the controlled 

human exposure studies dating back to the 1980’s. Studies where human volunteers are exposed 

to known concentrations of ozone in an experimental chamber are sometimes considered the 

gold standard in ozone research. Chamber studies have a number of advantages,213 including

known subject characteristics, precise measurement of pollutant concentration, elimination of 

confounding influences of temperature and other pollutants, precise measurement of effects, 

ability to assess acute and reversible effects, randomized and double blind designs, repeatability, 

temporal order of exposure and effects, and ability to demonstrate dose-response relationships.

At the same time, there are also substantial limitations with controlled human exposure 

studies, including:

 

213 J. Q. Koenig (1993). Health Effects of Ambient Air Pollution: How Safe is the Air We Breathe? Norwell, MA: 

Kluwer Academic Publishers (2000); W.F. McDonnell, Utility of controlled human exposure studies for assessing 

the health effects of complex mixtures and indoor air pollutants, Environ. Health Perspect., 101 Suppl 4: 199-203.
63

 Subjects are generally healthy, young adults-- not severely ill people or children;

 Only short-term exposures are feasible;

 Measurements must be minimally invasive; 

 The studies cannot directly examine a pollutant’s most severe effects;

 Inability to assess rare effects;

 Small number of subjects;

 Inability to study effects of repeated exposure;

 Statistical limitations of small sample size that make it difficult to detect small effects;

 Difficulty in studying complex pollutant mixtures;

 Homogeneous test subjects (generally healthy college students); and

 High costs to outfit laboratories and perform testing.

Of these limitations, several are of particular importance here. First, individuals tested in 

chamber studies are generally young, healthy, nonsmokers—that is, not children, not severely ill 

people, and not sensitive subpopulations. As discussed at length above, people with asthma, 

particularly children, have been found to be more sensitive and to experience larger decrements 

in lung function in response to ozone exposures than would healthy adults.214 Mudway et al.

2004 noted that since chamber studies use only healthy subjects, individuals with lung disease or 

other risk factors will experience responses at even lower levels.215 

Second, exposures in these studies were for 6.6 hours, not 8 hours. Ozone harm clearly 

increases with cumulative dose. A standard applying a longer exposure time than the study 

period, as EPA has previously used and proposed to use again for the ozone NAAQS, demands a 

lower level than that shown to induce adverse respiratory effects. In other words, if the study 

protocol is eliciting adverse effects at 80 ppb or 60 ppb after 6.6 hour exposures, a standard set 

for an 8-hour period must be somewhat lower than the level at which effects are observed 

because of the longer averaging time and greater accumulated dose of ozone. 

Third, the full range of human responses cannot be detected in studies with a small 

number of subjects. By using a small and select group, usually of young, healthy adults, the 

studies fail are generally unable to access the full range of human responses and individual 

sensitivity.

Fourth, chamber studies do not fully capture the potential adverse effects of real world 

outdoor ozone exposures that invariably occur in combination with other pollutants and 

environmental conditions that can exacerbate ozone’s harms. 

It is important to keep these strengths and limitations in mind when discussing the 

controlled human exposure studies of ozone. It is because of the studies’ limitations that it is also 

critical to consider evidence from other types of studies, including toxicological studies and 

epidemiological studies, in the discussion of health science. Consideration of all these types of 

 

214 Mortimer et al. 2002, supra note 85.

215 I.S. Mudway & F.J. Kelly (2004). An Investigation of Inhaled Ozone Dose and the Magnitude of Airway

Inflammation in Healthy Adults, Am. J. Respir. Crit. Care Med., 169: 1089-1095.
64

studies and evidence together, as in the ISA and by CASAC, provides the most complete picture 

of ozone-related health effects and physiological mechanisms. 

i. Controlled Human Exposure Studies Demonstrate 

Lung Function Decrements and Airway Inflammation 

at 60 ppb in Healthy Adults, as well as Pulmonary 

Inflammation, Injury, and Oxidative Stress

a. Lung Function Decrements and Airway 

Inflammation

Even in the 2008 review, there were several controlled human exposure studies that 

found evidence of harm from 6.6 hour exposures to 60 ppb ozone. Since the last review, several 

more important studies have been published reporting adverse effects at 70 ppb down to 60 ppb. 

In addition, two new models were been developed based on data from the controlled human 

exposure studies that make quantitative predictions of lung function response to ozone exposure 

and predict the degree of interindividual response to that exposure. This evidence demonstrates 

conclusively that the existing standard of 75 ppb (8 hour average) fails to protect public health. 

Four separate studies discussed in the ISA evaluate exposures to 60 ppb ozone: Kim et 

al. 2011216; Schelegle et al. 2009217; Adams 2002218; and Adams 2006219. These studies found

that ten percent of healthy young adults experience clinically significant declines in lung 

function when exposed for 6.6 hours to 60 ppb ozone, while engaged in moderate physical 

activity. Prolonged exposure to an average ozone concentration of 60 ppb results in group mean 

FEV1 decrements ranging from 1.8 percent to 3.6 percent.

220

 Based on data from these four 

studies, the weighted average group mean decrement was 2.7 percent. Some responsive subjects 

consistently experienced larger than average responses. This is important, as it provides insight 

into individual variable sensitivity, as discussed above. 

The Adams 2002 study reported that the results of an unreleased 1998 study revealed that 

“some sensitive subjects experience notable effects at 0.06 ppm.” This finding is based on the 

observation that 20 percent of the subjects exposed to 0.06 ppm ozone had a greater than 10 

percent decrement in FEV1. Even though the group mean response was not statistically different 

from the filtered air response, in a study with a small number of subjects the response of 

individual subjects is more important than the group mean response. This is particularly true for 

ozone exposure, where research has long recognized the variability in individual responses. 

 

216 C.S. Kim et al. (2011). Lung function and inflammatory responses in healthy young adults exposed to 0.06 ppm 

ozone for 6.6 hours, Am. J. Respir. Crit. Care Med., 183(9): 1215-21.

217 E.S. Schelegle, C.A. Morales, W.F. Walby, S. Marion , & R.P. Allen (2009). 6.6-hour inhalation of ozone 

concentrations from 60 to 87 parts per billion in healthy humans, Am. J. Respir. Crit. Care Med., 180(3): 265-72.

218 W.C. Adams (2002). Comparison of chamber and face-mask 6.6 hour exposures to ozone on pulmonary function 

and symptoms responses, Inhalation. Toxicol., 14: 745-764.

219 W.C. Adams (2006). Comparison of chamber 6.6-h exposures to 0.04-0.08 PPM ozone via square-wave and 

triangular profiles on pulmonary responses, Inhal. Toxicol, 18(2): 127-36.

220 Adams 2006 id.; Adams 2002, supra note 217; Schelegle et al. 2009, supra note 216; Kim et al. 2011, supra note 

215. 
65

A 2006 study by Adams showed respiratory symptoms and pain on deep inspiration, 

though did not find statistically significant lung function decrements at 6.6 hour exposures to 60 

ppb. However, though not reported by the original investigators, a reanalysis by Brown et al. 

2008221 of the Adams 2006 data reported that FEV1 decrements were highly statistically 

significant. As illustrated below in part A of Figure 3, the Brown et al. reanalysis found small, 

statistically significant declines in lung function using several common statistical tests, even after 

removal of three potential outliers. 

The Brown et al. reanalysis found that the statistical techniques used in the Adams 2006 

study were overly conservative for the evaluation of pre- to post-exposure changes in FEV1,

when comparing filtered air and ozone exposure. The reanalysis employed a standard approach 

used by other researchers. The pre- to post-exposure analysis showed that exposure to 60 ppb 

causes a small but statistically significant decrease in group mean FEV1 responses compared to 

filtered air, as illustrated in following figure. Brown et al. did not reanalyze Adams 2006’s 

respiratory symptoms data, but noted that Adams 2006 is “suggestive of an effect of 0.06 ppm on 

respiratory symptoms as well as FEV1.”222

While the average response is relatively small in these studies, it is important because this 

is an average response in a sample size limited to healthy, young adults and not sensitive 

populations. The data show considerable variability in lung function responses between similarly 

exposed subjects, with some individuals experiencing distinctly larger effects even when the 

group mean responses are small.

 

221 J.S. Brown, T.F. Bateson, & W.F. McDonnell (2008). Effects of exposure to 0.06 ppm ozone on FEV1 in 

humans: A secondary analysis of existing data, Env, Health Perspec., 116: 1023-1026. 

222 Id. at 1026.
66

Furthermore, when the Adams (2002, 2006) study data are corrected for the effect of 

exercise in clean air, 7 percent of subjects experience FEV1 decrements greater than 10 percent 

for ozone exposures of 0.04 ppm. Thirteen percent experience such decrements at 0.06 ppm,223

and 23 percent at 0.08 ppm, as shown by EPA.224 Larger decrements in FEV1 would be expected 

in more susceptible populations. Adams 2006 reported total symptom scores and pain on deep 

inspiration following 60 ppb exposures and group mean FEV1 responses during the 60 ppb 

exposures diverged from filtered-air and 40 ppb ozone exposures. The evaluation of pre- to postexposure effects on both total subjective symptoms and pain on deep inspiration are indicative of 

significant respiratory symptom effects at 60 ppb ozone. 

A more recent study, Schelegle et al. 2009 investigated the effect of 6.6-hour inhalation 

of ozone concentrations from 60 to 87 ppb in 31 healthy, young adults. Using a different 

statistical methodology than both Adams 2006 and Brown et al. 2008, this study reported 

statistically significant group mean FEV1 decrements of 6.1 percent at 70 ppb, and a statistically 

significant increase in respiratory symptoms (compared to those observed in filtered air) in 

healthy individuals. These findings dispel any remaining arguments that the current standard of 

75 ppb is protective of public health. The study also found decrements in lung function at 60 

ppb, of approximately the same magnitude as reported in the Adams studies. Sixteen percent of 

the subjects tested had lung function decrements greater than ten percent at 60 ppb.225

In an editorial commenting on the Schelegle et al. 2009 study, Brown noted: 

“There are at least three important findings from this study that have public 

health implications. First, statistically significant changes in FEV1 and symptoms 

occurred in healthy individuals at 70 ppb. Second, the magnitude of the mean 

FEV1 decrement (3.5% corrected for filtered air) at 60 ppb was about the same as 

reported by Adams. These findings further support a smooth dose-response curve 

without evidence of a threshold for exposures between 40 and 120 ppb O3. Third, 

consistent with numerous studies, there is considerable intersubject variability in 

response to O3. The distribution of response to O3 becomes skewed with 

increasing concentration, with a few individuals exhibiting large FEV1

decrements. Schelegle and colleagues found 16% of individuals to have greater 

than 10% FEV1 decrements at 60 ppb, and this proportion increased to 19, 29, 

and 42% at 70, 80, and 87 ppb, respectively.226

Most recently, Kim et al. 2011 investigated the effects of a 6.6-hour exposure to

60 ppb ozone during moderate exercise in young healthy adults. The study demonstrated 

statistically significant lung function deficits and inflammation compared to filtered air 

 

223 In reporting results at 0.06 ppm, Figure 21 below only includes information from Adams (2006). Adams (2002) 

at 747, 761, reported that 6 of 30 (or 20%) of subjects experienced FEV1 decrements ≥ 10% at 0.06 ppm. Thus, 8 of 

60 subjects (or 13%) experienced such decrements.

224 U.S. EPA (2007). Review of National Ambient Air Quality Standards for Ozone: Policy Assessment of Scientific 

and Technical Information, OAQPS Staff Paper (EPA-452/R-07-07), 3-7. 

225 Schelegle et al. 2009, supra note 216.

226 .S. Brown (2009). Acute Effects of Exposure to Ozone in Humans: How Low Can Levels Be and Still Produce 

Effects?, Am. J. Resp. Crit. Care Med., 180: 200-201.
67

exposures. Again, inflammation is an adverse health effect as discussed above. Unlike the 

earlier Adams 2006 and Schelegle et al. 2009 studies, which “were designed to compare multiple 

concentrations at multiple time points,” this study “was specifically designed to limit the need 

for multiple comparisons” and thus gets more directly at the question of what effect 6.6-hour 

exposure to 60 ppb ozone has on young healthy adults.227 In addition, this study provides 

important new evidence of airway inflammation, a mechanism by which ozone may cause other 

serious respiratory effects including asthma exacerbations. Persistent inflammation and injury, 

when observed in primate studies of chronic and intermittent exposure to ozone, is associated 

with remodeling of the airways.228 Though the earlier Adams and Schelegle et al. studies did 

not examine inflammation responses to ozone exposure, CASAC states that decrements of 10

percent FEV1 “are usually associated with inflammatory changes, such as more neutrophils in the 

bronchoalveolar lavage fluid.”229 Thus, inflammation likely resulted also from the exposures in 

those studies.

Given the results of these studies, the ISA’s conclusion that lung function is reduced at 60 

ppb--that “mean FEV1 is clearly decreased by 6.6-hour exposures to 60 ppb O3 and higher 

concentrations in [healthy, young adult] subjects performing moderate exercise”—is 

inescapable.230 Figure 6-1 of the ISA, below, illustrates that the group mean FEV1 responses at 

60 ppb fall on a smooth dose-response curve – without evidence of a threshold -- for exposures 

between 40 and 120 ppb ozone. 

Figure 3. ISA Figure 6-1- Cross-study comparison of mean ozone-induced FEV1 decrements 

following 6.6 hours of ozone exposure.

 

227 Kim et al. 2011, supra note 215, at 1218.

228 Guarnieri & Balmes 2014, supra note 75. 

229 Letter from CASAC Chair Dr. H. Christopher Frey to U.S. EPA Administrator Gina McCarthy re: CASAC 

Review of the EPA’s Health Risk and Exposure Assessment for Ozone (Second External Review Draft, February 

2014) (EPA-CASAC-14-005), 2, July 1, 2014 [hereinafter CASAC Letter 2014b] (response to charge questions, 

discussing HREA Fig.3-3).

230 ISA at 6-9.
68

Based on Adams 2002, Adams 2006, Schelegle et al 2009, and Kim et al 2011, the 

weighted average proportion of individuals with greater than ten percent FEV1 decrements is 10 

percent following 6.6 hours of exposure to 60 ppb ozone and 25 percent following exposure to 

80 ppb ozone.231 Ten percent of responders is an underestimate because some subjects 

experienced greater than ten percent decrements in lung function. Further, some responses are 

not corrected for filtered air exposures, during which lung function typically improves, which 

would therefore increase the size of the change, pre-and post-exposure.

232

 

A finding of 10 percent FEV1 decrements and pulmonary inflammation at 60 ppb 

necessitates a NAAQS standard no higher than 60 ppb for several reasons. First, it cannot be 

emphasized enough that these are tests of healthy adults, not sensitive populations like children 

or individuals with asthma. Second, as the studies themselves evince, there is a significant 

amount of variation in individual responses, meaning that in the general population, a large 

subset of healthy adults will have similar significant, enhanced responses.233 Third, and for these 

reasons, numerous authorities have concluded that such impacts constitute or are surrogates for 

adverse health effects.

For example, the American Thoracic Society views a 10 percent decrement in FEV1 as an 

abnormal response and a reasonable criterion for assessing exercise-induced 

 

231 Final Policy Assessment at 3-14; ISA at 6-18.

232 ISA sec. 6.2.1.1.

233 As discussed above, some people experience enhanced responses to ozone exposure. This is significant because 

extrapolating results of clinical chamber studies from a small number of subjects, where the intersubject variability 

is less than for the general population, to the larger population will likely results in larger numbers of more sensitive 

people. Indeed, Schelegle et al. 2009 and Kim et al. 2011 added to the previously available evidence for 

interindividual variability in the responses of healthy adults following exposures to ozone. As the proposal points 

out, following prolonged exposures to 80 ppb ozone while at moderate exertion, the proportion of healthy adults 

experiencing FEV1 decrements greater than 10 percent was 17 percent by Adams2006, 26 percent by McDonnell 

1996, and 29 percent by Schelegle et al. 2009. Following exposures to 60 ppb ozone, that proportion was 20 percent 

by Adams 2002, 3 percent by Adams 2006, 16 percent by Schelegle et al. 2009, and 5 percent by Kim et al. 2011.
69

bronchoconstriction.234 In previous NAAQS reviews, the EPA judged that for people with lung 

disease, moderate decrements in FEV1 of greater than 10 percent but less than 20 percent lasting 

up to 24 hours would likely interfere with normal activity for many individuals, and would likely 

result in more frequent use of medication.235 As discussed in Section IV.C above, more frequent 

use of medication is a change in clinical status that ATS considers to be adverse at the individual 

level. In the last review, CASAC advised that FEV decrements of 10 percent should be 

considered adverse in people with lung disease, especially children with asthma.236 CASAC has

stated that “[a] 10% decrement in FEV1 can lead to respiratory symptoms, especially in 

individuals with pre-existing pulmonary or cardiac disease. For example, people with chronic 

obstructive pulmonary disease have decreased ventilatory reserve (i.e., decreased baseline FEV1) 

such that a ≥ 10 percent decrement could lead to moderate to severe respiratory symptoms.”237 In 

this review, CASAC has again said that an “FEV1 decrement of ≥10% is a scientifically relevant 

surrogate for adverse health outcomes for people with asthma and lung disease.”238

b. Pulmonary Inflammation, Injury, and Oxidative 

Stress

In addition to lung function and respiratory impacts, controlled human exposure studies 

also demonstrate that ozone exposures can result in increased respiratory tract inflammation and 

epithelial permeability. Earlier controlled human exposure studies performed at concentrations of 

80 ppb and above frequently reported the presence of inflammatory markers such as 

polymorphonuclear neutrophils (PMNs) in the lungs. These neutrophils are the most abundant 

type of white blood cells in mammals. PMNs are recruited to the site of injury following trauma 

and are the hallmark of acute inflammation. 

The findings of the earlier human exposure studies were reinforced by a meta-analysis of 

21 human chamber studies where airway responses were assessed using bronchoscopy based 

lavage. Linear relationships were observed between ozone dose, airway inflammation, and 

protein leak into the airways over the early- and late-acute response time periods. Researchers 

found that exposure to 8-hour ozone concentrations of 0.08 ppm at moderate ventilation rates 

would be sufficient to trigger acute airway inflammation. The researchers noted that since 

chamber studies use only healthy subjects, individuals with lung disease or other risk factors will 

experience responses at even lower levels.239 In addition, most controlled human exposure 

studies have reported that people with asthma experience larger ozone-induced inflammatory 

responses than do people without asthma.240

 

234 ATS 2000. 

235 75 Fed. Reg. 2973 (Jan. 19, 2010). 

236 Letter from CASAC Chair Dr. Rogene Henderson to U.S. EPA Administrator Stephen L. Johnson on CASAC’s 

Peer Review of the Agency’s Final Ozone Staff Paper (EPA-CASAC-07-001), Oct. 24, 2006; Transcript of CASAC 

meeting, Aug. 24, 2006, at 149.

237 Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA Administrator Lisa P. Jackson on CASAC 

Response to Charge Questions on the Reconsideration of the 2008 Ozone National Ambient Air Quality Standards, 

(EPA-CASAC-11-004), Mar. 30, 2011.

238 CASAC Letter 2014a at 3. 

239 Mudway & Kelly 2004, supra note 214.

240 Policy Assessment at 3-19.
70

In the current review, inflammation has been demonstrated following 6.6 hour exposures 

to 60 ppb.241 Inflammation is a host response to injury, and the presence of inflammation an 

indication that injury has occurred.

Oxidative stress plays a key role in initiating and sustaining ozone-induced inflammation. 

The ISA explains that secondary oxidation products formed as a result of reactions between 

ozone and components of the epithelial lining fluid can increase the expression of cytokines and 

other molecules that enhance airway epithelium permeability.242 Ozone exposures can initiate an 

acute inflammatory response throughout the respiratory tract that has been reported to persist for 

at least 18-24 hours after exposure.243 The ISA notes that inflammation induced by ozone can 

have several potential outcomes:244

 It can resolve entirely; 

 Continued acute inflammation can evolve into a chronic inflammatory state and can alter 

the structure and function of other pulmonary tissue, leading to diseases such as asthma; 

 Inflammation can alter the body’s host defense response to inhaled microorganisms, 

particularly in potentially at-risk populations or lifestages such as the very young and old; 

and 

 Inflammation can alter the lung’s response to other agents such as allergens or toxins.

Lung injury and the resulting inflammation provide a mechanism by which ozone may 

cause serious health effects such as asthma exacerbations. CASAC concurs that “[s]uch changes 

may be linked to the pathogenesis of chronic lung disease.”245

Taken together, the chamber studies provide powerful evidence of the need to lower the 

8-hour ozone standard to 60 ppb or below. Clearly, EPA’s proposed standard of 65 to 70 ppb 

cannot be considered protective of public health in light of experimental evidence demonstrating 

adverse respiratory effects in healthy individuals exposed to 60 ppb, and the legal requirement to 

protect sensitive populations with an adequate margin of safety.

ii. New Models of Controlled Human Exposure Studies

Support Data Showing Adverse Health Impacts at 60 

ppb and Below

McDonnell et al. 2012246 and Schelegle et al. 2012247 developed models using data from a 

number of controlled human exposure studies on ozone exposure concentrations, ventilation 

rates, duration of exposures, and lung function responses. These models can make quantitative 

predictions of the potential lung function responses to ozone exposure, and the degree of 

 

241 Kim et al. 2011, supra note 215.

242 ISA sec. 5.3.3 and 5.3.4.

243 Id., sec. 6.2.3.

244 Id.

245 CASAC Letter 2014b at 2. 

246 W.F. McDonnell, P.W. Stewart, M.V. Smith, C.S. Kim, & E.S.Schelegle (2012). Prediction of lung function 

response for populations exposed to a wide range of ozone conditions, Inhal. Toxicol. 24(10): 619-33.

247 E.S. Schelegle, W.C. Adams, W.F. Walby, & M.S. Marion (2012). Modelling of individual subject ozone 

exposure response kinetics, Inhal. Toxicol., 24(7): 401-15.
71

interindividual variability. 

These studies analyzed large datasets from the controlled human exposure studies to fit 

compartmental models to estimate the dose of onset in lung function response, or a response 

threshold based upon the inhaled ozone dose. The McDonnell et al. 2012 model was fit to a 

dataset consisting of the FEV1 responses of 741 young, healthy adults (18-35 years of age) from 

23 different controlled exposure studies. Concentrations across individual studies ranged from 40 

ppb to 400 ppb, activity level ranged from rest to heavy exercise, and duration of exposure was 

from 2 to 7.6 hours. The Schelegle et al. 2012 model was fit to the FEV1 responses of 220 

healthy young adults from 21 controlled human exposure studies. The resulting responses to 

ozone in these studies were adjusted for responses observed following exposure to filtered air. 

The models estimate the frequency distribution of individual responses for various 

exposure scenarios and can provide summary measures of the distribution such as the mean or 

median response and estimates of the proportions of individuals with FEV1 decrements greater 

than 10, 15, and 20 percent. The dose is a function of exposure time as well as the level of 

exposure, as the models take into account the duration of exposure and level of oxidant stress in 

response to ozone exposure increasing over time as a function of dose rate, as well as decreasing 

over time by clearance or metabolization.

The results of the McDonnell and Schelegle models are consistent with real-life observed 

results from individual controlled human exposure studies of ozone-induced FEV1 decrements.248

In applying their model, McDonnell et al. 2012 estimated that 9 percent of healthy 

exercising adults would experience FEV1 decrements greater than 10 percent following 6.6 hour 

exposure to 60 ppb ozone, and that 22 percent would experience such decrements following 

exposure to 80 ppb ozone.249

Schelegle et al. (2012) estimated that, for 6.6 hours ozone exposure with moderate, 

exercise, the average dose of onset for FEV1 decrement would be reached following 4 to 5 hours 

of exposure to 60 ppb, and following 3 to 4 hours of exposure to 80 ppb. However, 14 percent of 

individuals in the Schelegle model began responding after one to two hours exposure to 50-80 

ppb ozone with moderate exercise. This estimate is consistent with the threshold FEV1

responses reported by McDonnell et al. 2012.250

CASAC judged these models as an advance over the exposure-response modeling 

approach used in the last review:251 

the comparison of the MSS [McDonnell-Stewart-Smith] model results to those 

obtained with the exposure-response (E-R) model is of tremendous importance. 

Typically, the MSS model gives results about a factor of three higher than the E-R 

model for school-aged children, which is expected because the MSS model 

 

248 See Policy Assessment at 3-15. 

249 ISA at 6-18, Fig. 6-3. 

250 Id. at 6-16.

251 CASAC 2014a at 7.
72

includes responses for a wider range of exposure protocols. 

In addition to the consensus letter and responses to the charge questions, each individual member 

of the CASAC panel filed additional individual comments that were appended to the letter. As 

an appendix to these comments, we include relevant excerpts from these individual comments 

because they provide detailed insight into CASAC’s rationale. 

Consistent with the data from published studies, this model predicts that 9 percent of 

healthy people would suffer FEV1 decrements greater than 10 percent and 1 percent of people 

would experience FEV1 decrements greater than 20 percent following 6.6 hour exposures to 60 

ppb ozone, clearly indicating the need for a standard of 60 ppb, or below. 

The exposure studies (and above-cited model based thereon) clearly demonstrate O3-

induced adverse effects at 60 ppb ozone. Those studies are both corroborated by, and provide 

biological plausibility to, the epidemiological studies and other evidence showing adverse effects 

at and about 60 ppb. Accordingly EPA must set the primary standard at (or below) that level. 

Lead Indus. Ass’n, 647 F.2d at 1153 (primary standard must “be set at a level at which there is 

‘an absence of adverse effect’ on [] sensitive individuals”). 

The models are consistent with the results of controlled human exposure studies finding 

adverse health impacts at 60 ppb. While the body of human exposure studies demonstrating lung 

function decrements and pulmonary inflammation at 60 ppb stand on their own and warrant a 

primary standard set at 60 ppb, these models provide significant additional support and verify the 

exposure study findings. 

Figure 4. ISA Figure 6-3-Proportion of individuals predicted to have FEV1 decrements following 

6.6-hour exposures
73

iii. New Research Confirms Additional Adverse Health 

Effects in Healthy Adults Exposed to Levels of 60 ppb 

for 6.6 Hours

Since the completion of the ISA, new information has been published reporting further 

analyses from the Kim et al controlled human exposure study at 60 ppb. This follow-up 

information provides important additional evidence of adverse health effects following 6.6 hour 

exposures to 60 ppb ozone. The new report provides additional measurements from the Kim et 

al controlled human exposure study including genotyping for genes reported to impact risk for 

responsiveness to ozone (GSTM1, NQO1, TNF), sputum cell assessment of markers of innate 

immune activation and function and inflammatory cells and cytokines.

Researchers reported that: 

individuals with an elevated PMN response to low level O3 are 13 times more 

likely of having the GSTM1null genotype than non-responders. Furthermore, 

responders have increased immuno-inflammatory responses to O3 compared to 

non-responders, and have elevated markers of inflammation following CA, 

suggesting the presence of a primed inflammatory airway in non-O3 exposed 

conditions. PMN responsiveness was also confirmed to be independent of the 

spirometric (FEV1) response to low level O3 in healthy people. 

As the researchers explained, “Since GSTM1 is a risk factor for asthma exacerbation and 

ozone, these data support the hypothesis that genetic modifiers of oxidative stress 

modulate the health effects of O3 in individuals with allergic airways disease.”252 

c. Epidemiological Studies Confirm Meaningful Associations 

Between Mortality, Morbidity and Ozone Exposure at Levels 

Of 70 ppb and Below

i. Findings from Short-Term Epidemiological Studies 

Compel a Standard of 60 ppb

Epidemiological studies evaluated in the ISA provide valuable information on morbidity 

and mortality associated with low-level exposures to ozone, and on exposure-response 

relationships. 

Many studies have demonstrated an independent association of short-term exposures of 

ozone to premature mortality, and respiratory and cardiac effects, often at mean or median 

concentrations of 60 ppb and below. 

 

252 N.E. Alexis et al. (2012). The Glutathione-S-Transferase null genotype and increased neutrophil response to low 

level ozone (0.06 ppm), J. Allergy Clin. Immunol., 131(2): 610-612,
74

The strengths and limitations of epidemiological studies complement those of the 

controlled human exposure studies in many ways:

 While the subjects in the chamber study are healthy young adults, epidemiological and 

panel studies can include sensitive populations in the natural environment. 

 Chamber studies can isolate the effect of a single pollutant, while real world exposures in 

epidemiological studies entail exposures to mixtures. 

 Controlled human exposure studies can focus on acute effects, while epidemiological 

studies can explore chronic effects and serious health endpoints such as hospitalization 

and mortality. 

As CASAC Chair Dr. Rogene Henderson aptly stated: 

“The epidemiology data showing increased use of medication, school absences, and 

hospital admissions is one way to evaluate the response of sensitive populations to ozone. 

The controlled human exposures gives you a ceiling level which is higher than the level 

that would be protective of sensitive populations.”

ii. The Current Standard is Not Protective of Public 

Health

EPA’s Policy Assessment highlights panel studies and epidemiological studies that were 

performed in areas that met the current air quality standard, or for multi-city studies, where the 

majority of locations would have met the current standard.253 

This approach provides compelling evidence that the current standard is not protective of 

public health. 

Table 3-2 from the Policy Assessment identifies five panel studies including a summer 

camp study of children, studies of outdoor workers, and studies of exercising adults that reported 

positive associations with lung function decrements and ozone concentrations of 75 ppb or 

below. 

 

253 Policy Assessment at 3-60–63. 
75

These studies provide compelling evidence that the current standard fails to protect public 

health. Several of them are discussed in more detail below. 

The study by Chan and Wu reported acute lung function decline in mail carriers exposed 

to ozone concentrations below the current ambient air quality standard.254 The 8-hour average 

concentration of ozone in this study was 36 + 12 ppb (mean + SD), and the maximum 8-hour 

concentration was 65.1 ppb. For a 10 ppb increase in the 8-hour average ozone concentration, the 

night peak expiratory flow rate was decreased by 0.54 percent for a 0-day lag, 0.69 percent for a 

1-day lag, and 0.52 percent for a 2-day lag. 

 

254 C. Chan & T. Wu (2005). Effects of ambient ozone exposure on mail carriers’ peak expiratory flow rates,

Environ Health Perspect, 113: 735-738.
76

The discussion in this paper pointed to earlier studies of adverse effects at concentrations 

below the current standard: 

“Because none of our study subject's daily O3 exposure exceeded the hourly 

standard of 120 ppb, our study supports previous findings from studies in the 

United States and Canada of a dose-response relationship between lung function 

change and O3 exposure at relatively low daytime ambient concentrations for 

healthy adults. Exercising healthy adults in New York City (USA) who were 

exposed to < 80 ppb O3 were reported to have a 0.55-L/min decrease in their 

PEFR per 1 ppb O3 (Spektor et al. 1988); healthy women exposed to 8-hr O3 at 

54 ppb in Connecticut and Virginia (USA) were reported to have a 0.083-

L/min/ppb decrease in their PEFR per 1 ppb O3 (Naeher et al. 1999); farm 

workers in Fraser Valley (Canada) who were exposed to a 1-hr daily maximum 

O3 of 40 ppb were reported to have 3.3-mL and 4.7-mL decreases in their FEV1.0 

and FVC, respectively, per 1 ppb O3 (Brauer et al. 1996). A similar doseresponse relationship between O3 and PEFR reduction was also reported in some 

European studies. Male cyclists in the Netherlands who were exposed to < 60 ppb 

O3 were reported to have 0.57-L/min decreases in PEFR per 1 ppb O3 

(Brunekreef et al. 1994); healthy workers and athletes in Germany who were 

exposed to < 80 ppb O3 were also reported to have decrements in their FEV1 

(Hoppe et al. 1995).”

Studies that excluded higher concentration days from the analysis that still find effects 

can provide very powerful evidence of effects at low concentrations. 

Brauer et al. (1996) is an important such study of the effect ozone exposure on lung 

function of outdoor farm workers undertaken in the Fraser Valley of British Columbia.255 The 

 

255

 M. Brauer, J. Blair, & S. Vedal (1996). Effect of ambient ozone exposure on lung function in farm workers, Am. 

J. of Resp. and Crit. Care Med., 154(4): 981-987.
77

mean daily maximum one-hour ozone concentration was 40 ppb (range: 13 to 84 ppb). 

Importantly, concentrations of acid aerosols and fine particulates, potential confounders of ozone 

effects, were very low. The study found that these exposures to ambient ozone were associated 

with decreased lung function over the day, which persisted to the following day. 

Even after excluding all days when the ozone was greater than 40 ppb, investigators still 

observed reduced lung function, demonstrating adverse effects at very low concentrations. 

Outdoor workers are the population most likely to have prolonged exposure to ambient ozone 

under conditions of exercise. The express value of this study is that it is one of the few to focus 

on outdoor workers, a population especially susceptible to ozone exposures and health effects. 

Brunekreef et al. (1994) is another such study that examined effects of ozone on a cohort 

of healthy young men who exercise outdoors—in this case, a group of amateur bicyclists in 

Netherlands.256 Researchers collected lung function measurements before and after training 

sessions or competitive races during the summer of 1991. Ozone concentrations were low on 

most occasions, with an average of just 43 ppb. Eight-hour ozone concentrations exceeded 50 

ppb only once during this study period, and concentrations of other pollutants were low. These 

low ozone concentrations were significantly associated with a decline in lung function over a 

race or training period. There was also an increase in respiratory symptoms, especially shortness 

of breath, chest tightness and wheeze in relation to ozone exposure. The effects persisted, even 

after removing all observations with hourly ozone greater than 60 ppb. This study provides vital 

evidence of the need for a 60 ppb standard or below. 

In a study of hikers at Mount Washington in New Hampshire, Korrick et al. (1998) 

evaluated the effects of acute ozone, PM2.5, and strong aerosol acidity on the pulmonary function 

of exercising adults.257 The mean 8-hour ozone concentration in this study was 40 ppb, and the 

maximum was 74 ppb. Lung function was measured before and after hiking, with the greatest 

responsiveness to ozone observed in those with asthma or wheezing, or in those who hiked 

longer. Hikers with a history of physician-diagnosed asthma or severe wheeze had a fourfold 

greater responsiveness to ozone than other hikers. Furthermore, the results found that a 

substantially increased fraction of the exercising population had significant declines in lung 

function (>10% declines in FEF 25-75%) on days with higher ozone.

Kinney et al (1996) used bronchoalveolar lavage to assess biomarkers of lung 

inflammation in recreational joggers exposed to relatively low doses of ozone in the New York 

City metropolitan area.258 Maximal hourly ozone concentrations on the day preceding the 

bronchoalveolar lavage ranged from 35 to 91 ppb, with a mean of 63 ppb. The average of daily 

maxima in the 7 and 28 days preceding the lavage were 56 ppb and 62 ppb, respectively. This 

study found that some of the individuals tested experience inflammation of the airways at 

concentrations of 60 ppb and below.

 

256 B. Brunekreef, et al. (1994). Respiratory effects of low-level photochemical air pollution in amateur cyclists, Am. 

J. of Resp. and Crit. Care Med., 150(4): 962-966.

257 S.A. Korrick et al.(1998). Effects of Ozone and Other Pollutants on the Pulmonary Function of Adult Hikers. 

Env. Health Perspec., 106: 93-99.

258 P.L. Kinney et al. (1996), Biomarkers of lung inflammation in recreational joggers exposed to ozone Am. J. of 

Resp. and Crit. Care Med., 154: 1430–1435.
78

iii. A Standard of 60 ppb is Needed to Protect Public 

Health

The Policy Assessment provides further analysis of additional studies that confirm 

evidence of harm at concentrations well below the current standard. 

Many areas of Canada have cleaner air than parts of the U.S., making Canadian studies 

especially useful for evaluating health effects of air pollution at relatively low concentrations. 

The Policy Assessment identifies five multi-city and one single city study that would likely have 

met various alternative standards under consideration. 

Shown below, Table 4-1from the Policy Assessment arrays information from these 

studies which reported that ozone is associated with an increased risk of hospital or emergency 

department visits for respiratory causes, or with premature death. The table shows that most of 

the study cities would have met a standard of 65 ppb during the entire study period, indicating 

that a standard of 65 would not be protective of public health. Even at 60 ppb, a number of study 

cities would have met the standard, suggesting that adverse effects persist at 60 ppb and that a 

lower standard is justified. 
79

These studies demonstrate serious adverse effects at low level exposures to ozone in the real 

world and they compel adoption of a final 8-hour average standard of 60 ppb. 

Mar and Koenig259 performed a time-series analysis using 1-hour and 8-hour ozone 

concentrations. They reported consistent positive associations across all lag times, with asthma 

emergency department visits for children in Seattle, a location that would have met the current 

standard over the entire study period. This analysis indicates that the current standard would 

allow concentrations of ozone shown to be associated with increased risk of respiratory 

emergency department visits for children. 

Single city studies also document a correlation between high ozone days and hospital

admissions for asthma. Silverman and Ito260, for example, demonstrate a 19 percent increase in 

intensive care unit asthma admissions in New York hospitals on high ozone days. School-aged 

children ages 6-18 with asthma consistently had the highest risk. The Silverman and Ito study of 

asthma hospital admissions of children in New York City reported positive associations with 

ozone, even when over 99 percent of the days would have had 8-hour maximum ozone levels 

below the level of the current standard. 

As illustrated in the figure below, the concentration-response relationship for ozone 

exposure and pediatric asthma emergency room visits in this study found no evidence of a 

threshold. Ozone concentrations as low as 30 ppb were associated with elevated rates of hospital 

admissions for asthma in children. 

 

259 T.F. Mar & J.Q. Koenig (2009). Relationship between visits to emergency departments for asthma and ozone 

exposure in greater Seattle, Washington, Annals of Allergy, Asthma, and Immunol., 103(6): 474-479. 

260 R.A. Silverman & K. Ito (2010). Age-related association of fine particles and ozone with severe acute asthma in 

New York City, J. Allergy Clin. Immunol., 125(2), 367-373.
80

Strickland et al.261 used population-weighting to combine daily pollutant concentrations across 

monitors in metropolitan Atlanta. The authors observed a 6.4 percent (95% CI: 3.2, 9.6%) 

increase in pediatric emergency room visits in hospitals throughout the metropolitan area, with a 

30 ppb increase in 8-hour maximum ozone concentrations in the at all-year analysis. Stronger 

associations were observed during the warm season. Ozone risk estimates were not substantially 

changed when controlling for other pollutants. The study found elevated associations with ozone 

at 8-hour maximum concentrations as low as 30 ppb, with no evidence of a threshold. 

 

261 M.J. Strickland et al. (2010). Short-term associations between ambient air pollutants and pediatric asthma 

emergency department visits, Am. J. of Resp. and Crit. Care Med., 182(3): 307-316.
81

Loess C-R estimates and twice-standard error estimates from generalized additive models 

for associations between 8-hour max 3-day average O3 concentrations and ED visits for 

pediatric asthma. Originally published in Strickland et al., 2010.

In the analyses of the studies by Silverman and Ito, the Policy Assessment discusses a 

range of “averaged” concentrations of 26 to 45 ppb where the studies found a high degree of 

confidence in the statistical association with emergency department visits for respiratory 

events.262 On more than 99 percent of the days when area-wide “averaged” ozone concentrations 

ranged from 26 and 45 ppb, the highest daily maximum 8-hour ozone concentrations were below 

75 ppb.263

The Policy Assessment states that an examination of the concentration-response 

relationship for ozone exposure and pediatric asthma emergency department visits found no 

evidence of a threshold with elevated associations with ozone at concentrations as low as 30 

ppb.

264

These studies, which examine the impact of real world exposures among one of the most 

at risk populations—children with asthma—provide strong support for a standard of 60 ppb.

 

262 Policy Assessment at 3-66-69. 

263 ISA at 3-67. 

264 Policy Assessment at 3.4.1.2, discussing Silverman and Ito 2010, supra note 259, and Strickland et al. 2010, 

supra note 260.
82

iv. Increased Evidence of Ozone-Caused Mortality in this 

Review

Substantial new information in this review supports earlier evidence that short-term exposures to 

ozone can increase the risk of premature death. Numerous epidemiological studies now have 

shown that short-term elevations in ozone pollution, particularly during the summer months, 

contribute to an increased risk of premature death, as illustrated in the following figure from the 

ISA. 

A significant body of strong, consistent evidence links short-term exposures to ozone to 

premature deaths. The substantiation rests in a growing number of epidemiological studies 

supplemented by emerging animal research providing evidence of biological plausibility. 

The ISA reports that a dozen newer multi-city studies and single-city studies, and several 

meta-analyses of these studies, have provided increased evidence for associations between shortterm ozone exposure and total mortality, even after adjustment for the influence of season and 

particulate matter. 

In summarizing the evidence, the Policy Assessment points to multi-city studies from the 

U.S. (Zanobetti and Schwartz 2008),

265, Europe (Samoli et al. 2009),266 Italy (Stafoggia et al.

 

265 A. Zanobetti & J. Schwartz (2008). Mortality displacement in the association of ozone with mortality: an analysis 

of 48 cities in the United States, Am. J. Respir. Crit. Care Med., 177 (2): 184-9.

266 E. Samoli et al. (2009). The temporal pattern of mortality responses to ambient ozone in the APHEA project, J. 

Epidemiol. Community Health; 63(12): 960-6.
83

2010),

267 and Asia (Wong et al. 2010),268 as well as a multi-continent study (Katsouyanni et al. 

2009)269, that report associations between short-term ozone exposures and mortality from 

respiratory causes.270 The studies of respiratory mortality during the summer ozone season were 

consistently positive, and most were statistically significant. 

The biological plausibility of the ozone-mortality link is supported by the experimental 

evidence of respiratory effects. The evidence cited in the ISA substantiates that increased risk of 

mortality is evident at levels well below the proposed standard. The study designs have taken a 

variety of approaches including single- and multi-city time series and case-crossover analyses. 

They have explored potential confounding by temperature, and other pollutants. The discussion 

below touches briefly on the results of those studies and emerging evidence of the possible 

biological mechanisms at work. The mounting evidence provides powerful support for selecting 

a standard no higher than 60 ppb.

Two critical multi-city studies published in 2004 show clear evidence of the ozonerelated mortality risk in the U.S. and Europe. Bell et al. published a large 14-year study of 

residents of 95 U.S. cities, in which short-term increases in ozone were found to increase total 

non-accidental mortality and deaths from cardiovascular and respiratory causes.271 A major 23-

city European study by Gryparis et al.272 reported a positive association between one- and eighthour concentrations of ozone air pollution and daily mortality, especially respiratory mortality, 

during the warm season. 

People may die from ozone exposure even when concentrations are well below the 

current standards. Bell and colleagues followed up on their 2004 multi-city study to estimate the 

exposure-response curve for ozone and risk of mortality and to evaluate whether a threshold 

exists below which there is no effect.273 They applied several statistical models to data on air 

pollution, weather, and mortality for 98 U.S. urban communities for the period 1987-2000. The 

results provide strong and consistent evidence that daily changes in ozone pollution are linked to 

premature death. The ozone and mortality results do not appear to be confounded by 

temperature or PM10. 

Significantly, as indicated in the figure below, the relationship between mortality and 

ozone was evident even on days when pollution levels were well below 60 ppb. 

 

267 M. Stafoggia (2010). Susceptibility factors to ozone-related mortality: a population-based case-crossover 

analysis, Am. J. Respir. Crit. Care Med., 182(3): 376-84.

268 Wong et al. (2010). Part 5. Public health and air pollution in Asia (PAPA): a combined analysis of four studies of 

air pollution and mortality. Res. Rep, Health Eff. Inst., (154): 377-418.

269 K. Katsouyanni (2010). Air pollution and health: a European and North American approach (APHENA). Res. 

Rep, Health Eff. Inst., (142): 5-90.

270 Policy Assessment at 3-35 – 36. 

271 M.L. Bell et al. (2004). Ozone and short-term mortality in 95 US urban communities, 1987-2000, JAMA, 292: 

2372-2378.

272 A. Gryparis et al. (2004). Acute effects of ozone on mortality from the "air pollution and health: a European 

approach" project, Am. J. Respir. Crit. Care Med., 170 (10): 1080-7.

273 M.L. Bell et al. (2006). The Exposure-Response Curve for Ozone and Risk of Mortality and Adequacy of Current 

Ozone Regulations, Environ. Health Perspect., 114(4): 32-536.
84

Exposure Response Curve for ozone and mortality using the spline approach: percentage 

increase in daily nonaccidental mortality at various ozone concentrations. Originally 

published in Bell, et al. 2006, taken from Bell, ML “Recent Evidence on the Relationship 

between Ozone and Mortality,” Presentation to the Estimating Mortality Risk Reduction Benefits 

from Decreasing Tropospheric Ozone Exposure Panel, National Research Council on March 29, 

2007. 

Zanobetti and Schwartz (2011) conducted a large multicity study of 48 U.S. cities and 

reported a positive association between ozone and all-cause mortality during the summer 

months.274 The researchers found that ozone was also associated with deaths from 

cardiovascular disease, strokes, and respiratory causes. Mean 8-hour ozone concentrations in the 

study ranged by city from 15.1 to 62.8 ppb. The 75th percentile 8-hour ozone concentrations 

ranged from 19.8 ppb in Honolulu to 75.9 ppb in Los Angeles. 

Franklin and Schwartz (2008) studied 18 U.S. communities and reported an association 

between summertime ozone levels and non-accidental mortality.275 This association was robust 

to the inclusion of PM2.5 in the analysis, strengthening confidence in the ozone-mortality link. 

The researchers concluded that the association of ozone with daily deaths in the summer does not 

represent short-term mortality displacement and is an issue of public health concern. The study 

found that the impact of ozone on mortality was reduced when sulfate exposures were also taken 

into account. Average daily ozone concentrations in the study ranged by community from 21.4 

in Seattle to 48.7 ppb in Fresno. 

Meta-analyses offer compelling evidence that these ozone-mortality findings are 

consistent. Four meta-analyses completed between 2001 and 2004 reported evidence that ozone 

 

274 A. Zanobetti & J. Schwartz (2008). Mortality displacement in the association of ozone with mortality: an analysis 

of 48 cities in the United States, Am. J. Respir. Crit. Care Med., 177 (2): 184-9.

275 M. Franklin & J. Schwartz (2008). The impact of secondary particles on the association between ambient ozone 

and mortality, Environ. Health Perspect.,116: 453-458. 
85

contributes to early death.276 Three independent analyses in 2005 used statistical techniques to 

synthesize the results of different studies of ozone and mortality. Separate research groups from 

Johns Hopkins University, Harvard University, and New York University conducted independent 

meta-analyses, using their own study selection criteria and methods. All three meta-analyses 

reported a remarkably consistent link between daily ozone levels and total mortality.277,278,279 

The results of these meta-analyses are summarized in the figure below, which illustrates the 

consistency in the findings. 

Results of the Meta-Analyses studies. From Bell, ML. “Recent Evidence on the Relationship 

between Ozone and Mortality,” Presentation to the Estimating Mortality Risk Reduction Benefits 

from Decreasing Tropospheric Ozone Exposure Panel, National Research Council on March 29, 

2007.

 

276 J.I. Levy (2001). Assessing the Public Health Benefits of Reduced Ozone Concentrations. Environ. Health 

Perspect., 109: 1215-1226; G.D. Thurston & K. Ito K.(2001). Epidemiological Studies of Ozone Exposures and 

Acute Mortality, J. Exposure Analysis and Environ. Epidemiology, 11: 286-294; H.R. Anderson et al. (2004). MetaAnalysis of Time-Series Studies and Panel Studies of Particulate Matter (PM) and Ozone (O3). Report of a WHO 

Task Group. Copenhagen: World Health Organization; D.M. Stieb, S. Judek, & R.T. Burnett (2002). Meta-analysis 

of time-series studies of air pollution and mortality: Effects of gases and particles and the influence of cause of 

death, age and season. J .Air & Waste Manage Assoc., 52: 470-84.

277 M.L. Bell, F. Dominici, & J.M. Samet (2005). A Meta-Analysis of Time-Series Studies of Ozone and Mortality 

with Comparison to the National Morbidity, Mortality, and Air Pollution Study. Epidemiology, 16: 436-445. 

278 J.I. Levy, S.M. Chermerynski, & J.A. Sarnat (2005). Ozone Exposure and Mortality: An Empiric Bayes 

Metaregression Analysis, Epidemiology, 16: 458-468. 

279 K. Ito, S.F. De Leon, & M. Lippmann (2005). Associations Between Ozone and Daily Mortality: Analysis and 

Meta-Analysis. Epidemiology, 16: 446-429. 
86

Analyses clearly indicate that the death effect of ozone is distinct from the effect of 

temperature and particle pollution. Bell et al. (2007)280 analyzed the effect of PM on the 

association between short-term exposure to ozone and mortality, using data from 98 U.S. 

communities. By estimating the correlation between daily PM and ozone concentrations, and 

including PM as a covariate in various models, Bell et al. concluded that neither PM10 nor PM2.5 

is a likely confounder of the observed relationship between ozone and mortality. 

A case-crossover study of 14 U.S. cities was designed to control for the effect of 

temperature on daily deaths.281 The study concluded that the association between ozone and 

mortality risk reported in the multi-city studies is unlikely to be due to confounding by 

temperature. 

v. Biological Mechanisms

Evidence is emerging on biological mechanisms. A review article offers possible 

mechanisms for altered morbidity and mortality associated with ozone air pollution, related to a 

complex interaction with the innate immune system.282 

As shown in the figure below, inhalation of ozone impairs antibacterial defense in many 

types of cells in the lung. Ozone can disrupt the epithelial barrier and mucociliary clearance and 

can induce production of proinflammatory factors. Ozone is directly cytotoxic to macrophages. 

Ozone can modify macrophage phagocytosis of microbial pathogens, intracellular killing, and 

levels of secreted factors. 

 

280 M.L. Bell, J.Y. Kim, & F. Dominici (2007). Potential confounding of particulate matter on the short-term 

association between ozone and mortality in multisite time-series studies. Environ. Health Perspect., 115(11): 1591-

5.

281 J. Schwartz (2005). How sensitive is the association between ozone and daily deaths to control for temperature? 

Am. J. Resp. Crit. Care Med., 171: 627- 631. 

282 J.W. Hollingsworth, S.R. Kleeberger, & W.M. Foster (2007). Ozone and Pulmonary Innate Immunity. Proc. Am. 

Thorac. Soc., 4: 240-246.
87

An animal study takes this research further. Hollingsworth and colleagues found that 

ozone shuts down the responses of the immune system in the lungs of mice, making them more 

responsive, and therefore more vulnerable to infections and diseases.283 Ozone primes the 

immune system to hyper-respond and destroys some of the protective immune cells, leaving the 

lungs vulnerable to later bacterial infections. 

vi. Confidence in the Associations Shown Does Not 

Decrease at 60 ppb

EPA specifically posted this question to the CASAC: 

“To what extent does your confidence that the effects observed in epidemiological studies 

are attributable specifically to O3 lessen or otherwise change, if at all, at the lower levels 

in the proposed range [60-70 ppb] as compared to the higher levels?” 

CASAC’s unanimous response to this question belies EPA’s assertion that that there is 

increased uncertainty of effects at lower levels such as 60 ppb:284

“While epidemiological studies are inherently more uncertain as exposures and risk 

estimates decrease (due to the greater potential for biases to dominate small effect 

estimates), specific evidence in the literature does not suggest that our confidence on the 

 

283 J.W. Hollingsworth et al. (2007). Ambient Ozone Primes Pulmonary Innate Immunity in Mice. J. Immunology, 

179: 4367-4375

284 Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA Administrator Lisa P. Jackson on CASAC 

Response to Charge Questions on the Reconsideration of the 2008 Ozone National Ambient Air Quality Standards, 

(EPA-CASAC-11-004), 10, Mar. 30, 2011

Illustration of possible 

mechanisms for ozone 

interaction with cells in the 

lungs. From Hollingsworth et al 2007.
88

specific attribution of the estimated effects of ozone on health outcomes differs over the 

proposed range of 60-70 ppb. In framing our answer to this question, we note that the 

range covered is quite narrow and we would not anticipate major differences in the 

characteristics of the pollution mixture across this range.” 

Regarding the epidemiological studies, the Committee went on to state its concern for effects 

ranging from increased risk of morality to lung function declines: 

“Several distinct classes of epidemiological studies are relevant in this range and some 

examples are given below. For instance, mortality effects for ozone have been found in 

time-series studies in communities where mean ambient concentrations are well below 

the proposed range (e.g., Vedal et al 2003). Exercise-induced decrements in lung 

function, known to be causally related to ozone in controlled exposure studies, have been 

observed in field studies of healthy volunteers. For instance, in a cross-sectional study, 

Korrick et al. (1998) found that hikers on Mount Washington experienced significant 

decreases in FEV1 after prolonged exercise on days when ozone averaged 40 ppb (range 

21 to 74 ppb). The magnitude of these decrements increased as mean ozone levels 

increased and it was nearly fourfold higher for persons with asthma than for persons 

without asthma. Panel studies of campers are yet another class of field studies that have 

shown effects on children’s lung function are associated with ambient ozone. For 

example, in a panel of healthy children, Spektor et al. (1988) showed significant 

reductions in FEV1 associated with one-hour average ambient ozone, even when 

restricted to days with ozone below 60 ppb. Similarly, in panels of children with 

moderate to severe asthma attending summer camp, Thurston et al. (1997) reported not 

only respiratory function changes, but also more clinically significant responses, 

including increases in physician prescribed rescue medication and respiratory symptoms. 

In yet another class of epidemiological studies, health care utilization for asthma has 

been shown to decrease when ozone concentrations decreased. For example, Friedman et 

al (2001) found that during the Summer Olympic Games in Atlanta in 1996 there was 

significantly decreased use of pediatric care for asthma that correlated best with a 

reduction in peak ozone concentrations. In this study, the relative risk of asthma events 

increased stepwise at cumulative ozone concentrations 60 to 89 ppb and 90 ppb or more 

compared with ozone concentrations of less than 60 ppb. The reduction of the adverse 

effects on asthma in this study was dependent on reduction of ozone exposures to levels 

below 60 ppb.” 

“Our confidence that the effects from epidemiological studies are attributable to ozone is 

also bolstered by the recognition that the endpoints of concern do not change at the

lower levels of the proposed range. While it may be difficult to disentangle the effect of a 

single pollutant in epidemiological studies, the evidence regarding ozone-related health 

effects from epidemiological studies is consistent with the evidence from controlled 

exposure studies that involve ozone alone. Indeed, evidence from observational studies of 

individuals exercising outdoors indicates ozone may have even stronger lung function 

effects than those estimated in controlled exposure studies, suggesting the possibility that 

a mixture of photochemical oxidants may be more toxic than ozone alone. Finally, 

whether or not the effects attributed to ozone in epidemiological studies are specific to 
89

ozone vs. the entire photochemical oxidant pollutant mixture, it is likely that reductions in 

population exposures to ozone will result in fewer adverse health effects. Our confidence 

in this statement does not change at the lower levels of the proposed range.”285

vii. Effects Persist Even After Excluding High 

Concentration Days above a Certain Level 

Studies that find positive effects after excluding days above a certain concentration provide 

compelling evidence of associations evident at low concentrations and are especially pertinent to 

the setting of air quality standards. Some important examples include: 

 Brunekreef et al. 1994286: Even after removing all observations with hourly ozone 

concentrations greater than 60 ppb, researchers found a decline in lung function and an 

increase in respiratory symptoms in this group of amateur cyclists. 

 Brauer et al. 1996287: Even after excluding all days when the ozone was greater than 40 

ppb, investigators still observed reduced lung function in a cohort of outdoor workers. 

 Mortimer et al. 2002288: After excluding days when 8-hour average ozone was greater 

than 80 ppb, the associations with morning lung function decrements remained 

statistically significant. 

 Bell et al. 2004289: Estimates of premature mortality attributable to ozone changed little 

when days with 24-hour average concentrations greater than 60 ppb were excluded. 

 Bell et al. 2006290: There was little difference in the mortality effect estimate when days 

with 24-hour ozone concentrations above 20 ppb were excluded. 

 Spektor et al. (1988)291: Statistically significant reductions in FEV1 were associated with 

one-hour average ambient ozone, even when restricted to days with ozone below 60 ppb.

viii. EPA Must Base Standards on Concentrations 

Below the Mean in Epidemiological Studies 

 

285 Id. at 10-11.

286 B. Brunekreef, et al. (1994). Respiratory effects of low-level photochemical air pollution in amateur cyclists, Am. 

J. of Resp. and Crit. Care Med., 150(4): 962-966.

287 M. Brauer, J. Blair, & S. Vedal (1996). Effect of ambient ozone exposure on lung function in farm workers, Am. 

J. of Resp. and Crit. Care Med., 154(4): 981-987.

288 K.M. Mortimer, L.M. Neas, D.W. Dockery, S. Redline, & I.B. Tager (2002). The effect of air pollution on innercity children with asthma. Eur. Respir. J., 19(4): 699–705.

289 M.L. Bell et al. (2004). Ozone and short-term mortality in 95 US urban communities, 1987-2000, JAMA, 292: 

2372-2378.

290 M.L. Bell et al. (2006). The Exposure-Response Curve for Ozone and Risk of Mortality and Adequacy of Current 

Ozone Regulations, Environ. Health Perspect., 114(4): 32-536. 

291 D.M. Spektor, et al. (1998). Effects of ambient ozone on respiratory function in active, normal children, Am. 

Rev. of Resp. Disease, 137(2): 313-320.
90

EPA must interpret the epidemiological studies to set a standard that is protective of 

public health with an adequate margin of safety. 

Many short-term epidemiological studies that find positive associations with adverse 

respiratory health outcomes report air quality concentrations as a mean or median metric of 

varying time periods: 1-hour; 8-hour; or 24-hour. The mean concentrations reported as a 

summary statistic in many studies and summarized in numerous tables in Chapter 6 of the ISA, 

do not tell the whole story. That is because adverse effects are occurring along a continuum of 

ozone concentrations. 

CASAC made this point strongly in its November 6, 2012 letter292:

“The epidemiologic studies should be used to draw inferences regarding the shape and 

magnitude of the concentration-response functions between ozone exposures and various 

health outcomes across the full range of the ozone exposure distribution. An important 

consideration will be the level of confidence in the concentration-response functions for 

concentrations in the range of interest, especially 60 to 70 ppb and perhaps below 60 

ppb. With this approach, the EPA can utilize information from various studies regardless 

of whether the way in which ozone was assessed directly matches the form or averaging 

period used in the standard. The purpose is to infer the general causal relationship (i.e., 

shape of and magnitude of the concentration-response function) between exposure levels 

and risk of various outcomes. As noted above, even studies performed in locations that 

did not meet the current standard may provide useful information on the relationship 

between ozone and health across the entire distribution of ozone.” 

CASAC member Dr. Ana Diez Roux293 elaborated on this point in her individual comments on 

the draft Policy Assessment: 

In several places the chapter notes that selected epidemiologic studies that were 

conducted in cities that would not have met the current standard provide no insight into 

the appropriateness of the degree of public health protection provided by the current 

standard (this statement is made several times in reference to both short term and long 

term exposure studies). This seems an overstatement. The informativeness of these studies 

depends on the actual distribution and range of ozone concentrations investigated rather 

than on whether the standard was or was not met. To the extent that these studies allow 

estimation of the dose-response gradient extending into the ozone exposure distribution 

that would be expected even if the current standard were met, they do indeed provide 

important evidence that can be used to determine the health benefit that could be 

 

292 Dr. Chris Frey, Chair, Clean Air Scientific Advisory Committee and Dr. Jonathan M. Samet, Immediate Past 

Chair, Clean Air Scientific Advisory Committee, Letter to the Honorable Lisa P. Jackson, Administrator, U.S. 

Environmental Protection Agency, re CASAC Review of the EPA’s Policy Assessment for the Review of the 

National Ambient Air Quality Standards (First External Review Draft—August 2012). EPA-CASAC-13-003, 

November 26, 2012.

293 Frey and Samet letter, November 26, 2012 – Appendix A – Comments of Dr. Ana Diez Roux.
91

expected if the standard were lowered even further.

CASAC panel member Ed Avol agreed294: 

“I agree that there is data from recent epidemiological investigations on which to 

consider exposure distributions across the entire O3 concentration range, and it would 

be informative to do so, and I do think there is interesting and important information to 

consider at ranges below the existing standard.”

In considering the results reported for epidemiological studies, EPA has to look at the 

distribution of air quality values. Adverse effects are occurring at concentrations both above and 

below the mean. The bulk of the effects occur within one standard deviation of the mean. One 

standard deviation below the mean in the most relevant statistic to consider for standard setting 

purposes, because it reflects the lower end of the distribution of air quality values where adverse 

effects are occurring. 

Most epidemiological studies report mean concentrations and the distribution of air 

quality values around the mean. EPA must use this information to set a standard that provides an 

adequate margin of safety. The highest concentration day in a study is not the appropriate metric 

upon which to base the level of the standard. 

While the current form of the ozone standard is based on the average of the fourth highest 

daily max over three years, the level should be set based on the full distribution of the air quality 

data reported in the epidemiological studies. 

In addition to the numerous studies discussed above, a number of other epidemiological 

and field studies have reported effects of acute exposures to ozone at concentrations less than 60 

ppb. These studies report positive, statistically significant effects of acute ozone exposure on 

lung function, respiratory symptoms, and cardiovascular outcomes, daily emergency department 

visits, daily hospital admissions, and mortality. 

These comments cite statistics drawn from the studies themselves of mean and sometimes 

maximum ozone concentrations. This information is can be very useful to inform the standardsetting process. Depending on the study design, a variety of statistics may be reported, for 

example 1-hour maximum, 8-hour average, 24-hour average, or various percentile 

concentrations. 

ix. Many Additional Epidemiological Studies Show Need 

for 60 ppb Standard

Additional epidemiological studies demonstrate that a standard at least as stringent as 60 

ppb is needed to protect against a range of serious adverse health impacts. This review considers 

substantial evidence showing the effects of ozone on hospital admissions and emergency 

department visits. 

 

294 Frey and Samet Letter, Nov. 26, 2012 - Appendix A – Comments of Ed Avol.
92

A very large case-crossover study of Medicare recipients in 36 U.S. cities evaluated the 

effect of ozone and PM10 on respiratory hospital admissions in the elderly over a 13-year 

period.295 Medina-Ramón, et al found that the risk of daily hospital admissions for chronic 

obstructive pulmonary disease (COPD) and pneumonia increased with short-term increases in 

ozone concentrations during the warm season, but not during the cold season. Importantly, 8-

hour mean warm season ozone concentrations in this study ranged from 15 ppb in Honolulu to 

63 ppb in Los Angeles. As indicated in the table below, concentrations in most cities were in the 

40-55 ppb range. This study provides powerful evidence for a standard 60 ppb or below. 

 

295 M. Medina-Ramón, A. Zanobetti, & J. Schwartz (2006). The Effect of Ozone and PM10 on Hospital Admissions 

for Pneumonia and Chronic Obstructive Pulmonary Disease: A National Multicity Study, Am. J. of Epid, 163: 579-

588.
93

Medina-Ramón, et al.2006

A large study in Atlanta by Tolbert et al.296 found a positive association between shortterm ozone exposure (mean 8-hour ozone concentration 53.0 ppb) and respiratory disease-related 

emergency visits during non-winter months. This association remained robust in multipollutant 

models.

Similarly, Wilson et al (2005) found that ozone increases in New England were 

correlated with emergency room visits for asthma in Portland, Maine, but not in Manchester, 

New Hampshire, a smaller city with fewer visits to analyze. The maximum 8-hour mean ozone 

concentration in Portland was 43.1 ppb (13.5 SD).297 

Yang et al. (2007) reported positive associations between ozone and hospital admissions 

for COPD in Taipei, Taiwan in single- and two-pollutant models. Mean ozone concentrations 

were 20.52 ppb, and maximum ozone concentrations were 62.79 ppb in this study.298 

In a study published last year, researchers in Stockholm, Sweden total used ten years of 

data from the Swedish cardiac arrest register with a time-stratified case-crossover design to 

analyze exposure to air pollution and the risk of out-of-hospital cardiac arrest.299 Exposure to 

ozone, PM2.5, PM10, NO2, and NOx was defined as the mean urban background level during 0–2, 

0–24, and 0–72 hours before the event and control time points. After adjusting for temperature 

and relative humidity, Raza et al found that ozone was associated with an increased risk of outof-hospital cardiac arrest for all time windows analyzed. The mean 8-hour maximum ozone 

concentration in urban areas during the warm season was just 34 ppb. 

The study suggests that short-term elevations of ozone urban background levels are 

associated with an increased risk of out-of-hospital cardiac arrest with no indication of a 

threshold, in a region with 23 ppb 24-hour mean ozone levels. 

 

296 Tolbert et al. (2007). Multipollutant modeling issues in a study of ambient air quality and emergency department 

visits in Atlanta, J. Expo. Sci. Environ. Epidemiol., 17 Suppl. 2: S29-35.

297

 A.M. Wilson (2005). Air Pollution, Weather, and Respiratory Emergency Room Visits in Two Northern New 

England Cities: an Ecological Time-Series Study, Environ, Res., 97: 312 -321.

298

 C.Y. Yang & C.J. Chen (2007). Air pollution and hospital admissions for chronic obstructive pulmonary disease 

in a subtropical city: Taipei, Taiwan, J. Toxicol. Environ. Health, 70: 1214-1219. 

299 A. Raza, et al. (2014). Short-term effects of air pollution on out-of-hospital cardiac arrest in Stockholm, Eur. 

Heart J., 35 (13), 861-8.
94

From Raza, et al. 2014.

Additional studies document evidence of harm at levels well below both the existing 

standard and the proposed range. Not surprisingly, most provide additional evidence of the risks 

faced by vulnerable populations at low levels of exposure. A number of these studies are 

discussed in more detail below. 

x. Studies of Infants, Children, and the Elderly

Epidemiological studies of effects of low concentrations of ozone on infants, children, 

and adults over age 65 indicate not only that the current standards do not protect these sensitive 

populations and need to be lowered, but document harm to these populations at levels well below 

the EPA proposal.

Triche et al (2006) examined respiratory effects of ozone in 700 infants living in 

nonsmoking households in southwestern Virginia.300 The authors concluded: 

 

300 E.W. Triche et al. (2006). Low-level ozone exposure and respiratory symptoms in infants, Environ Health 

Perspect., 114 (6): 911-6.
95

“At levels of ozone exposure near or below the current U.S. EPA standards, infants are 

at increased risk of respiratory symptoms, particularly infants whose mothers have 

physician-diagnosed asthma.” 

Although the “current” 8-hour standard in 2006 was the equivalent of 84 ppb (0.08 parts 

per million), the conclusion still holds true today. In this study there were no days when the onehour standard was exceeded, and only two days when the 8-hour ozone standard was exceeded. 

As shown in the following table, the mean 8-hour maximum ozone concentration was 54.5 ppb, 

with a standard deviation + 13.0.

Dales et al. studied 15 years of data on newborns 0-28 days of age in 11 large Canadian 

cities to determine the influence of gaseous air pollutants on neonatal respiratory disease.301 

Daily hospitalizations for respiratory causes were correlated with daily concentrations of ambient 

air pollutants. Results were adjusted for day of the week, temperature, barometric pressure, and 

relative humidity. As illustrated in the following table, ozone concentrations were extremely low 

in this study, ranging from a 24-hour mean level of 13.3 ppb in Vancouver to 23.1 ppb in Saint 

John, with a population weighted average of 17 ppb. Effects evident at these low concentrations 

strongly suggest the need for a final standard of 60 ppb or below. 

A

study of the impact of ozone on daily respiratory admissions on children less than three years old 

and another sensitive population, the elderly, in Vancouver, British Columbia revealed 

associations between ozone and respiratory hospital admissions, which persisted after adjustment 

 

301 R.E. Dales, S. Cakmak, & M.S. Doiron (2006). Gaseous Air Pollutants and Hospitalization for Respiratory 

Disease in the Neonatal Period, Environ. Health Perspect., 114: 1751-1754.
96

for copollutants and socioeconomic status.302 The 24-hour average ozone concentrations in this 

study were very low at 13.4 ppb. 

Important evidence of the increased sensitivity of children with asthma also comes from 

two studies by Mortimer and colleagues. They examined the effect of daily ambient air pollution 

in a cohort of 864 asthmatic children in 8 urban areas of the U.S. in a longitudinal study. The 

cities studied were Baltimore, Chicago, Cleveland, Detroit, Bronx/East Harlem, St. Louis, and 

Washington DC. Eight-hour average ozone concentrations from 10 a.m. to 6 p.m. were 48 ppb. 

Median concentrations across cities ranged from 34 to 58 ppb.303 Researchers found that 

summertime air pollution at levels below the current air quality standards was significantly 

related to symptoms and decreased pulmonary function in children with asthma. Ozone was 

most influential on peak expiratory flow rate. Adverse respiratory effects were observed in all 

cities. This compelling provides strong support for an 8-hour ozone standard of 60 ppb or below. 

A follow-up study of the same cohort found that asthmatic children born prematurely or 

with low birth weight have the greatest response to ozone.304 Scientists sought to ascertain 

which subgroups in a cohort of 846 inner-city asthmatic children aged 4-9 years old were most 

susceptible to the effects of summertime ozone. Children were recruited from emergency 

departments and primary care clinics the eight U.S. cities. Mean 8-hour ozone concentrations 

from 10 a.m. to 6 p.m. across these cities was 48 ppb, as shown in the figure below. The study 

reported that "children of low birth weight or of premature birth are at greater risk for respiratory 

problems, and appear to be substantially more susceptible to the effects of summer air pollution 

than children of normal birth weight or full-term gestation." 

 

302 Q. Yang et al. (2003). Association between ozone and respiratory admissions among children and the elderly in 

Vancouver, Canada, Inhal, Toxicol, 15(13): 1297-308.

303 K.M. Mortimer, L.M. Neas, D.W. Dockery, S. Redline, & I.B. Tager (2002). The effect of air pollution on innercity children with asthma. Eur. Respir. J., 19(4): 699–705.

304 K.M. Mortimer, I.B. Tager, D.W. Dockery, L.M. Neas, & S. Redline (2000). The effect of ozone on inner-city 

children with asthma: identification of susceptible subgroups, Am. J. Respir. Crit. Care Med., 162(5): 1838-1845.
97

Mortimer et al., 2000.

Additional evidence of the increased sensitivity of asthmatic children is provided by the 

study by Gent et al. Yale University researchers studied a group of 271 asthmatic children under 

age 12, living in Connecticut and Springfield, Massachusetts in a prospective study of asthma 

severity.305 The children’s mothers tracked their asthma symptoms such as wheeze, persistent 

cough, chest tightness, and shortness of breath, and their medication use, on a daily basis. The 

study found that children with severe asthma were at significantly increased risk due to ozone, 

even after controlling for co-exposure to fine particles, and at pollution levels well below the 

current EPA air quality standards for ozone. According to the study, “An ozone level of 63.3 

ppb or higher (same-day 8 hour average) was associated with a 30% increase in chest tightness. 

Previous day levels of 52.1 ppb or above were associated with chest tightness, persistent cough 

and shortness of breath." This study also provides evidence of the sensitivity of asthmatic 

children on maintenance medication to ozone, and of the need to lower the standard due to 

effects at low concentrations. As indicated in the following table, mean 8-hour ozone 

concentrations in this study were 51.3 ppb, with a standard deviation of 15.5. 

 

305 J.F. Gent et al. (2003). Association of Low-Level Ozone and Fine Particles with Respiratory Symptoms in 

Children with Asthma. JAMA, 290(1): 1859-1867.
98

Gent et al., 2003. 

Tolbert et al. examined pediatric emergency room visits for asthma in relation to air 

quality.306 As shown in the following table, mean 8-hour ozone concentrations in this study 

were 59.3 ppb, with a standard deviation of 19.1. Ozone was found to be associated with asthma 

emergency room visits, with a relative risk of 1.026 per 20 ppb ozone. Associations were robust 

to analytical method and model specifications. The authors conclude that both ozone and PM10

are independently associated with asthma exacerbation, and that the data “suggest continuing 

health risks at pollution levels that commonly occur in many US cities.” This study provides 

strong evidence of the need to set the 8-hour average standard at 60 ppb. 

Tolbert et al., 2000.

Babin et al in a 2007 study reported associations between pediatric emergency 

department visits and outdoor ozone concentrations are strongest for school-age children 5-12 

years old. In this group, a 1 ppb increase in ozone concentration indicated a mean 3.2 percent 

increase in daily emergency department visits, and a mean 8.3 percent increase in daily 

 

306 P.E. Tolbert (2000). Air Quality and Pediatric Emergency Room Visits for Asthma in Atlanta, Georgia, Am. J. 

Epidemiol., 151: 798-810. 
99

emergency admissions for asthma exacerbations. The 8-hour daily maximum ozone 

concentrations reached Code Red levels on only five days during the study period.307

xi. Two Important New Studies Published Since the 

Completion of the ISA Provide Additional Support for 

a 60 ppb Standard

Two studies published after the completion of the ISA provide strong new evidence of 

adverse effects at concentrations of 60 ppb or below. 

A study in Sublette County, Wyoming, an area of concentrated oil and gas drilling, 

explored the association between daily ozone concentrations and visits to primary care clinics for 

respiratory problems.308 Sublette County had been reporting high ozone levels in the winter. 

Pride and colleagues reported that for every 10-ppb increase in the 8-hour maximum 

average ground-level ozone, there was a three percent increase in clinic visits the following day. 

The effect was strongest during the winter months. Furthermore, the mean 8-hour maximum 

ozone concentrations ranged from 41 ppb to 53 ppb among the monitoring stations included. 

The results were consistent when days with ozone concentrations greater than 75 ppb were 

excluded. This provides powerful evidence that clinic visits for respiratory causes increase even 

on days when the ozone is lower than the current standard of 75 ppb. 

 

307 Babin et al. (2007). Pediatric patient asthma-related emergency department visits and admissions in Washington, 

DC from 2001-2004, and associations with air quality, socio-economic status and age group. Environ. Health, 21: 6-

9.

308 K.R. Pride (2014). Association of short-term exposure to ground-level ozone and respiratory outpatient clinic 

visits in a rural location - Sublette County, Wyoming, 2008-2011. Environ Res., 137C: 1-7.
100

Table from Pride et al., 2014.

The Framingham Heart Study is a large cohort study of adult men and women in the 

Boston, Massachusetts area.309 For this study, Rice and colleagues used the Air Quality Index 

values to examine the effect of low levels air pollution, within the current NAAQS, on lung 

function within this well-studied cohort. The study measured lung function with previous days’ 

exposure to ozone (among other pollutants). 

Exposure to pervious days’ ozone concentrations in the “moderate” range was associated 

with lung function declines of 55.7 ml lower FEV1, compared to days when the air quality was in 

the “good” range. According to the authors, these findings suggest that “the general population, 

not just ‘unusually sensitive’ people, may experience respiratory effects from ambient pollution 

at levels that are considered to be safe.” This important finding underlines the broad public 

health risks of ozone at the current standard level. 

The table shows that mean 8-hour ozone concentrations in this study were 28.7 ppb, with 

a range of 2 to 59.6 ppb. In other words, lung function declines occurred despite ozone 

concentrations having never exceeded 60 ppb over the course of the study. 

 

309 M.B. Rice, et al. (2013). Short-term exposure to air pollution and lung function in the Framingham Heart Study, 

Am. J. Respir. Crit. Care Med., 188(11), 1351-7.
101

Table from Rice et al (2014) showing air pollutants and relevant meteorological conditions.

Under the current Air Quality Index, air quality is rated in the “good range,” when 8-hour 

average concentrations are less than 59 ppb. The “moderate range” is from 60 to 75 ppb, below 

the current NAAQS. 

xii. EPA Analysis Shows that Numerous Studies Have 98th

Percentile 8-hour Daily Maximum Concentrations 

Below 70, 65, and 60 ppb

In the last review, our organizations filed comments310 identifying twenty North 

American studies which reported positive, statistically significant results for various health 

endpoints, for which EPA derived 98th percentile 8-hour daily maximum concentrations of about 

85 ppb or lower.311 The studies in Table 5 below, are drawn from Appendix 3B of the 2007 Staff 

Paper.312 Even where the areas studied would have met the 98th percentile form of alternative 

standard levels below 70 ppb, adverse health effects were observed at those lower levels.

EPA argues that the 98th percentile statistic may be relevant to standard-setting because 

it approximates the 4th highest daily maximum concentrations averaged over 3 years. As such, 

the studies indexed in the Table 5 provide additional evidence for a standard of 60 ppb. 

It is noteworthy that five studies report positive, statistically significant relationships 

between 8-hour ozone concentrations and various adverse effects at concentrations below 60 

ppb, seven additional studies (for a total of 12) report effects below 70 ppb. 

 

310

 Comments of American Lung Association, Environmental Defense, and Sierra Club on U.S. EPA’s Proposed 

Revisions to the National Ambient Standards for Ozone, 72 Fed. Reg. 37,818 (Oct. 9, 2007).

311 L. McCluney, M. Rizzo, & R. Ross (2006). Development of descriptive statistics for 8-hr daily maximum ozone 

data from epidemiologic studies. U.S. EPA Memorandum to Ozone NAAQS Review Docket (OAR-2005-0172).

312 U.S. EPA (2007). Review of National Ambient Air Quality Standards for Ozone: Policy Assessment of Scientific 

and Technical Information, OAQPS Staff Paper (EPA-452/R-07-07). 
102
103

Ozone Epidemiological Studies Showing Effects at Low Concentrations: EPA Derived 98th 

Percentile Statistics Near or Below the Current Standard 

Source: American Lung Association, 2007, Derived from Staff Paper Appendix 3B. Ozone 

Epidemiological Study Results: Summary of effect estimates and air quality data reported in 

studies, distribution statistics for 8-hr daily maximum ozone concentrations for the study period 

and location, and information about monitoring data used in the study.

In short, taking into consideration all the available evidence, from the short-term 

epidemiological studies, commenters find overwhelming evidence of the need for a 8-hour 

average standard of at least 60 ppb. 

xiii. Findings from Long-Term Epidemiological 

Studies Compel a Standard of 60 ppb

As discussed above, controlled human exposure studies, while critical to understanding 

the adverse health effects of ozone exposure, nonetheless have a number of limitations that can 

work to understate the effects that real world ozone exposures can have on human health. 

Epidemiological studies included in this review cycle support the ISA’s new, stronger 

conclusion that there is a likely causal relationship between long-term exposures to ozone and 

respiratory effects. The ISA finds that “...long term ozone exposure is associated with adverse 

effects ranging from episodic respiratory illness to permanent respiratory injury to progressive 

respiratory decline.”313 The ISA document details numerous studies showing that long-term 

exposures to ozone are associated with new onset asthma, increased asthma symptoms, increased 

risk of asthma hospital admissions, deficits in lung function growth rate in children, and 

increased risk of premature death. 

Many of the studies reported average ozone concentrations in the range of 60 to 70 ppb or 

below. Different exposure metrics are used in different studies. Some authors report the 

maximum 1-hour average within a 24-hour period, others report the maximum 8-hour average 

within a 24-hour period, and others report the 24-hour average. 

xiv. Increased Premature Mortality from Long-Term 

Exposures

Jerrett et al. used data from the American Cancer Society Cancer Prevention Study II on 

449,000 participants to examine the effect of long-term exposures to air pollution on mortality 

from cardiopulmonary causes in 96 metropolitan areas.314 Investigators reported significant 

increase in the risk of death from respiratory causes, but not from cardiovascular causes, in 

association with an increase in ozone concentration, even after accounting for PM2.5 and other 

factors. The average ozone concentration for each metropolitan area during the interval from 

1977 to 2000 ranged from 33.3 ppb to 104.0 ppb during the summer months.

 

313 ISA sec. 7.2.8 

314 M. Jerrett et al. (2009). Long-term ozone exposure and mortality, New Eng. J. of Med., 360(11): 1085-1095.
104

Average ozone concentrations in three-quarters of the metropolitan areas were less than 62.5 

ppb, and less than 57.4 ppb in half the MSAs. The map below indicates where the high and low 

pollution areas were located. 

This table shows the number of MSAs in each of the ozone exposure categories. 

The risk of dying from respiratory causes was more than three times as great in the metropolitan 

areas with the highest ozone concentrations compared to those with the lowest ozone 

concentrations. 
105

A principal finding of the Jerrett study was that ozone and PM each contributed 

independently to the increased risk in premature death. The effect of ozone on mortality was 

insensitive to adjustment for individual, neighborhood, and metropolitan-area confounders or to 

differences in multilevel-model specifications. 

The figure below, from the Jerrett study, shows that risk of premature death from ozone 

exposure rose sharply when daily maximum one-hour ozone concentrations were approximately 

55 ppb. Since the Jerrett study examined the daily maximum one-hour concentrations, this 

would indicate that even a lower 8-hour average would provide increased risk of premature 

death.

While expressing some reservations, CASAC concurred that Jerrett et al. (2009) “is an 

appropriate study to use at this time as the basis for the long-term mortality risk estimates given 

its adequacy and the lack of alternative data.”
106

xv. Long-Term Exposure and Survival Rate in People with 

Pre-existing Conditions

A recent study by Zanobetti and Schwartz investigated whether long-term exposure to 

ozone was associated with survival in four cohorts of Medicare enrollees with specific diseases 

in 105 United States cities.

315

 Investigators reported an increased risk of death for persons with a 

history of congestive heart failure, myocardial infarction, chronic obstructive pulmonary disease, 

and diabetes associated with each 5 ppb increase in summer average ozone concentrations. 

These findings are consistent with Jerrett et al that longer-term exposure to ozone is associated 

with reduced survival. 

xvi. Long-Term Exposures and New Onset Asthma

Prospective cohort studies have reported an association between ozone exposures and 

asthma induction. These studies suggest that ozone may not only exacerbate asthma, but may 

also trigger the development of the disease. 

The ASHMOG prospective cohort study of over 3,000 adults in the nonsmoking Seventh 

Day Adventist community sought to examine the whether long-term exposure to ozone air 

pollution can contribute to the prevalence of asthma. The study found that 8-hour average 

ambient ozone concentration averaged over a 20-year period was associated with doctor 

diagnoses of adult-onset asthma in nonsmoking males.316 

The Children’s Health Study is a long-term cohort study designed to examine whether 

long-term exposure to air pollution was related to chronic respiratory effects in children in 12 

southern California communities. McConnell et al 2010317 reported an increased risk for new 

onset asthma in children living in communities with the highest ozone concentrations (59.8 ppb 

annual average of 8-hour daily average ozone) compared to the community with the lowest 

ozone concentration of 29.5 ppb. A follow-up study by Islam et al 2008318 examined evidence of 

a genetic predisposition to develop asthma, and observed a dose-response relationship from the 

low pollution community (38.4 ppb) to the high pollution community (55.2 ppb). 

Another analysis from the California Children’s Health Study points strongly to ozone as 

a cause in the development of asthma in young people who did not previously have the disease. 

The study compared new asthma cases in 3,535 children who were followed over five years in 

12 Southern California communities to determine the potential health damage caused by growing 

 

315 A. Zanobetti & J. Schwartz (2011). Ozone and survival in four cohorts with potentially predisposing diseases, 

Am. J. Respir. Crit. Care Med., 184(7): 836-41.

316 W.F. McDonnell, D.E. Abbey, N. Nishino, & M.D. Lebowitz (1999). Long-term ambient ozone concentration 

and the incidence of asthma in nonsmoking adults: the AHSMOG study, Environ. Res., 80(2), 110-121.

317 R. McConnell et al. (2010). Childhood incident asthma and traffic-related air pollution at home and school. 

Environ. Health Perspect., 118(7): 1021-1026 .

318 . Islam, et al. (2008). Ozone, oxidant defense genes, and risk of asthma during adolescence, Am. J. Respir. Crit. 

Care Med., 177 (4): 388-95.
107

up in polluted air. Six of the communities had higher than average ozone concentrations while 

six had lower than average concentrations. 

As noted by Pinkerton et al., this study found that "the incidence of new diagnoses of 

asthma in children who exercise heavily is associated with average ozone levels of 55.8 to 69.0 

ppb during the daytime (10 a.m. to 6 p.m.), levels below the current NAAQS."319 The study 

found that children in the high ozone communities who played three or more sports developed 

asthma at a rate three times higher than those in the low ozone communities. Because 

participation in some sports can result in a child drawing up to 17 times the “normal” amount of 

air into the lungs, young athletes are more likely to develop asthma.320

xvii. Asthma Hospital Admissions in Children

Lin et al 2008321 examined the association between long-term ozone concentrations and 

first asthma hospital admission for New York children in a retrospective cohort study. The study 

 

319 .E. Pinkerton, J.R. Balmes, M.V. Fanucchi, & W.N. Rom (2007). Ozone, a malady for all ages. Am. J. Respir. 

Crit. Care Med., 176: 107-8.

320 R. McConnell et al. (2002). Asthma in exercising children exposed to ozone: A cohort study, Lancet, 359(9304): 

386-391. 

321 S. Lin, X. Liu, L.H. Le, & S. Hwang (2008). Chronic exposure to ambient ozone and asthma hospital admissions 

among children, Env. Health Perspect., 116(12): 1725-1730.
108

reported three chronic exposure indicators: annual average of 8-hour maximum ozone 

concentrations (41 ppb), ozone season average (50.6 ppb) and proportion of follow-up days with 

ozone levels greater than 70 ppb. Hospital admissions for asthma were significantly associated 

with increased ozone levels for each of the chronic exposure indicators in a dose-response 

relationship. 

xviii. Asthma Emergency Department Visits and 

Hospital Admissions

Meng et al322 used California Health Interview Survey data to study the association 

between air pollution and asthma morbidity in the San Joaquin Valley of California, an area with 

high asthma rates. Authors reported increased asthma-related emergency department visits or 

hospitalization in association with ozone in all age groups. Median annual ozone concentrations 

(based on hourly data) were 30.3 ppb, with a 25-75 percentile range of 27.1 to 34 ppb. Potential 

confounding by PM was ruled out in this study. 

Table 7-2 in the ISA details the annual mean concentration as well as the range of ozone 

concentrations for selected key new studies regarding ozone and respiratory health effects. 

Many of the studies in this table report low mean or median annual concentrations, and low 

 

322 Y,Y, Meng et al. (2010). Outdoor air pollution and uncontrolled asthma in the San Joaquin Valley, California, J. 

Epidemiol. Comm. Health, 64(2): 142-7.
109

maximum or 75th percentile concentrations. These data must be considered in evaluating the 

suitability of averaging time and level of the ozone standard. 

xix. Long-Term Exposures and Asthma Prevalence

A study in Los Angeles and San Diego counties investigated associations between traffic 

and outdoor air pollution levels near residences, and poorly controlled asthma in adults. This 
110

study reported that annual average ozone exposures were associated with poorly controlled 

asthma among elderly adults.323

xx. Low Levels of Ozone over the Long-Term Stunt Lung 

Function Growth in Children

A number of studies have provided evidence that long-term exposure and relatively low 

concentrations may have detrimental effects on full development of lung capacity in growing 

children. 

Frischer et al. followed a group of 1,150 first and second grade children in two counties 

in Austria from 1994-1996, to investigate the long-term effects of ambient ozone.324 The highest 

and lowest exposure to ozone differed by a factor of two. Researchers found small but consistent 

decrements in lung function associated with ambient ozone. They conclude: "This is the first 

study that suggests chronic effects of ozone on lung function growth in children. Thus, ozone 

would constitute a risk factor for premature respiratory morbidity during later life." This effect of 

ozone was confirmed in a follow-up study.325 

Galizia et al. examined data from health status questionnaires and lung function 

measurements in relation to residence histories to examine the effect of long-term ozone 

exposures on over 500 non-smoking Yale college students. Investigators found that "living for 

four or more years in regions of the country with high levels of ozone and related copollutants is 

associated with diminished lung function and more frequent reports of respiratory symptoms."326

Künzli et al. developed a protocol to relate lifetime cumulative ozone exposure to small 

airway pulmonary function. This study included 130 nonsmoking, non-asthmatic freshmen from 

the University of California at Berkeley who were lifelong residents of the Los Angeles Basin or 

the San Francisco Bay Area, who had volunteered to participate in lung function testing. 

Researchers observed declines in mid- and end-expiratory flow measures of the small airways 

that are considered early indicators for pathologic changes that might ultimately progress to 

chronic obstructive lung disease. These declines were associated with estimated long-term ozone 

exposures.327

A follow-up study assessed effects of chronic exposure to air pollutants in University of 

California, Berkeley freshmen who were lifelong residents of the Los Angeles or San Francisco 

Bay areas. Students in the study had never smoked. Air pollution exposure was estimated based 

 

323 Y,Y. Meng, M. Wilhelm, R.P. Rull, P. English, & B. Ritz (2007). Traffic and outdoor air pollution levels near 

residences and poorly controlled asthma in adults, Ann. Allergy Asthma Immunol., 98, 455-463. 

324 T. Frischer et al. (1999). Lung Function Growth and Ambient Ozone: A Three-Year Population Study in School 

Children, Am. J. Respir. Crit. Care Med., 160: 390-396.

325 F. Horak et al. (2002). Particulate Matter and Lung Function Growth in Children: A 3-yr Follow-up Study in 

Austrian Schoolchildren, Eur. Respir. J., 19, 838-845.

326 A. Galizia & P.L. Kinney (1999). Long-Term Residence in Areas of High Ozone: Associations with Respiratory 

Health in a Nationwide Sample of Nonsmoking Young Adults, Environ. Health Perspect., 107(8): 675-679.

327 N. Künzli, et al. (1997). Association between Lifetime Ambient Ozone Exposure and Pulmonary Function in 

College Freshmen: Results of a Pilot Study, Environ Res., 72(1): 8-23.
111

on spatial interpolation of PM10, nitrogen dioxide, and ozone monitors to the students residences. 

Lung function measurements were gathered between February and May, when the students had 

not had recent exposure to increased levels of ozone. The study found that lifetime exposure to 

ozone in adolescents 18-20 years old is associated with reduced levels of lung function measures 

that reflect the function of the small airways. The associations are independent of any effects 

related to PM and nitrogen dioxide.328

The California Children’s Health Study annually measured the lung function of 1,700 

fourth-graders enrolled in 1996, monitored the communities' air pollution for four years until 

2000, and analyzed the relationships between their lung function growth and the levels of six 

pollutants. Exposure to ozone was correlated with reduced growth in peak flow rate. Larger 

deficitsin lung function growth rate were observed in children who reported spending more time 

outdoors. Slower lung growth over a period of several years is evidence of a chronic effect of air 

pollution on children's respiratory health. Children whose lungs have grown more slowly may 

have lower maximum lung function as adults, making them more susceptible to respiratory 

diseases and chronic problems as they age.329

A study of over 3,000 8-year old children followed for 3 years in Mexico City underlines 

the concern about the effects of long-term exposures. After adjusting for acute exposure and 

other potential confounders, deficits in (forced vital capacity) FVC and FEV1 growth over the 

three year follow-up period were significantly associated with exposure to ozone and other 

pollutants in girls and boys. Over the course of the study period, 8-hour average ozone 

concentrations ranged from 60 ppb to 90 ppb. In multipollutant models, an interquartile range 

increase in mean ozone concentration of 11.3 ppb was associated with an annual deficit in FEV1

of 12 ml in girls and 4 ml in boys. Early lung function deficits may increase the risk of 

developing chronic obstructive pulmonary disease later in life, as well increasing the risk of 

cardiovascular morbidity and overall mortality.330 

Researchers compared chest x-rays from children living in heavily polluted southwest 

Mexico City with children living in a cleaner air region in Tlaxcala, Mexico. Ozone 

concentrations exceeded the U.S. NAAQS for an average of 4.7 hours per day, and PM2.5

concentrations were above the annual standard. The x-rays of the Mexico City children showed 

an increased prevalence of bilateral hyperinflation and increased linear markings. CT scans of 

25 Mexico City children with abnormal chest x-rays showed evidence of mild bronchial wall 

thickening, prominent central airways, air trapping, and pulmonary nodules in some of the 

children, findings suggestive of inflammatory processes. Testing showed 7.8 percent of the 

Mexico City children had abnormal lung function.331 

xxi. Chronic Ozone Exposure and Lung Damage

 

328 I.B. Tager, et al. (2005). Chronic Exposure to Ambient Ozone and Lung Function in Young Adults, 

Epidemiology, 16(6): 751-759.

329 W.J. Gauderman (2000). Association between Air Pollution and Lung Function Growth in Southern California 

Children: Results from a Second Cohort, Am. J. Respir. Crit. Care Med., 162: 1383–1390.

330 R. Rojas-Martinex et al. (2007). Lung Function Growth in Children with Long-Term Exposure to Air Pollutants 

in Mexico City, Am. J. Respir. Crit. Car Med., 176: 377-384. 

331 L. Calderón-Garcidueňas et al. (2006). Lung Radiology and Pulmonary Function of Children Chronically 

Exposed to Air Pollution, Environ. Health Perspect., 114: 1432-1437.
112

Researchers found that the air pollution exposure produces significant chest X-ray 

abnormalities in the exposed children, depressed lung function, and an imbalance of blood 

proteins important to immune response. Twenty-two percent of the exposed children had grossly 

abnormal nasal mucosa, which can impair nasal defense mechanisms against inhaled gases and 

particles. The lung damage observed is similar to the chronic inflammatory damage observed in 

an earlier study of dogs in Mexico City. Researchers report that the x-ray and lung function 

changes they found in the exposed children could be due to pollution-associated chronic 

bronchiolitis, which could put the children at greater risk of developing chronic obstructive 

airway disease later in life. They conclude that lifelong exposure to urban air pollution causes 

respiratory damage in children and may predispose them to development of chronic lung disease 

and other problems due to suppression of the immune system.332

xxii. Pathological Changes to Nasal Passages

Another study by some of the same researchers reported that biopsies taken from these 

children exhibit a wide range of pathologic changes to the cells of the nasal passages. 

"The severe structural alteration of the nasal epithelium together with the 

prominent acquired ciliary defects are likely the result of chronic airway injury in 

which ozone, particulate matter, and aldehydes are thought to play a crucial role," 

concluded the researchers. "The nasal epithelium in SWMMC [Southwest 

Metropolitan Mexico City] children is fundamentally disordered, and their 

mucocilliary defense mechanisms are no longer intact. A compromised nasal 

epithelium has less ability to protect the lower respiratory tract and may 

potentially leave the distal acinar airways more vulnerable to reactive gases."333 

xxiii. Remodeling of the Airways in Toxicology Studies 

of Primates

Animal toxicology studies have demonstrated that chronic exposure to ozone air 

pollution may result in inflammation and injury leading to interstitial remodeling that “may play 

an important role in the progression and development of chronic lung disease.”334 

xxiv. A Standard of 60 ppb or Below is Needed to 

Protect Against Long-Term Exposures

Despite the wealth of scientific information on long-term ozone exposures and their 

adverse impacts reviewed in the ISA, EPA fails to rationally explain how its proposed primary 

standard will assure prevention of such adverse impacts 

 

332 L. Calderón-Garcidueñas et al. (2003). Respiratory Damage in Children Exposed to Urban Pollution, Pediatric 

Pulmonology,; 36: 148-161.

333 L. Calderón-Garciduenas et al. (2001). Ultrastructural Nasal Pathology in Children Chronically and Sequentially 

Exposed to Air Pollutants, Am. J. Resp. Cell Molec. Bio., 24: 132-138.

334 ISA sec. 7.2.4.
113

Specifically, EPA must consider whether the current form and level of the standard 

assures the absence of long-term ozone-induced adverse effects. The Policy Assessment looks at 

the Jerrett et al. study and the HREA using a function from the Jerrett study to estimate 

premature respiratory deaths attributable to long-term exposures to ozone air pollution. 335

As EPA explains: 

With regard to long-term O3 concentrations, compared to the current standard or 

a revised O3 standard with a level of 65 or 70 ppb, a revised standard with a level 

of 60 ppb would be expected to further reduce the risk of respiratory mortality 

associated with long-term concentrations, based on information from the study by 

Jerrett et al. (2009).[153] In addition, a standard with a level of 60 ppb would be 

expected to more effectively maintain long-term O3 concentrations below those 

where the study by Jerrett et al. (2009) indicates the most confidence in the 

reported association with respiratory mortality.

Specifically, air quality analyses indicate this to be the case in all of the urban 

study areas evaluated at a level of 60 ppb, compared to 6 out of 12 areas for the 

current standard, 9 out of 12 for a standard with a level of 70 ppb, and 10 out of 

12 for a standard with a level of 65 ppb (U.S. EPA, 2014c, Table 4-3). Finally, a 

revised standard with a level of 60 ppb would be expected to further reduce longterm O3 concentrations based on the types of metrics that have been reported in

recent epidemiologic studies to be associated with respiratory morbidity (i.e., 

seasonal averages of daily maximum 8-hour concentrations).336

Thus EPA’s own assessment indicates that a standard of 70 ppb would be effective in limiting 

long-term exposures shown to increase the risk of premature death in only 9 of 12 urban study 

areas, and a standard of 65 ppb would do so in only 10 out of 12 areas. Of the options analyzed, 

only a standard of 60 ppb would eliminate dangerous exposures in all 12 study areas. 

Fundamentally, EPA’s proposal argues that an 8-hour average standard of 70 or 65 ppb 

would reduce long-term ozone concentrations and therefore mortality risks compared to the 

current standard, but fails to acknowledge that millions would be left unprotected at a standard of 

70 or 65. 

The fact that EPA places “less weight” on epidemiological-based risk estimates does not 

equate to a finding that such estimates are not entitled to material weight. EPA must protect 

against the adverse effects shown in the epidemiological studies and associated risk estimates 

unless the agency finds based on reasoned analysis that above-cited factors render the results so 

unreliable as to make them not credible. EPA has made no such finding here, and the record 

would not support such a finding. The fact that the Jerrett results are from only one study does 

not undermine their credibility, particularly given EPA’s finding that the study was welldesigned. And the fact that the Jerrett study did not identify a clear threshold does not 

undermine the PA finding of “a relatively high degree of confidence in the linear concentration-

 

335 See Policy Assessment at 3-75; see HREA at 7-6.

336 Proposed Rule at 75,302.
114

response function for ‘long-term’ ozone concentrations at least as low as 56 ppb...”337 EPA 

cites338 the following language from the CASAC letter: 

In light of the potential nonlinearity of the C–R function for long-term exposure 

reflecting a threshold of the mortality response, the estimated number of premature 

deaths avoidable for long-term exposure reductions for several levels need to be viewed 

with caution.

But CASAC also found: 

In terms of quantitative risk assessment, the most relevant scientific evidence 

available is with respect to epidemiologic estimates of the relationship between 

ambient concentration and mortality. Thus, EPA’s risk assessment appropriately 

focuses on this particular heath end point for long-term exposure. 339 

Taken together, these statements simply mean that CASAC felt the precise numerical estimates 

of deaths avoidable should be viewed with caution 

Further, in response to EPA’s claim that most of the study areas would have violated the 

current standard, we note that there is a linear concentration-response relationship at least down 

to 56 ppb, and possibly below. 

The Policy Assessment also notes that: 

a revised standard with a level of 60 ppb would be expected to further reduce 

long-term O3 concentrations based on the types of metrics that have been reported 

in recent epidemiologic studies to be associated with respiratory morbidity (i.e., 

seasonal averages of daily maximum 8-hour concentrations).

EPA must set the 8-hour standard with a margin of safety sufficient to prevent long-term 

exposures to ozone that are likely to cause chronic adverse effects on lung capacity, and other 

respiratory health endpoints, including premature death. 

The currently available information on long-term effects shows the need for an 8-hour 

standard of 60 ppb, at the lower end of the range recommended by CASAC and EPA staff 

scientists. The primary standard must “be set at a level at which there is ‘an absence of adverse 

effect’ on [] sensitive individuals” such as children, the elderly, and people with respiratory 

illnesses. Lead Indus. Ass’n v. EPA, 647 F.2d 1130, 1153 (D.C. Cir. 1980). The long-term 

studies cited above show that adverse effects are likely at ozone levels at and above 60 ppb: 

Accordingly, the primary standard must be set at a level no higher than 60 ppb. 

 

337 Policy Assessment at 3-76.

338 Proposed Rule at 75,277, n. 85, citing CASAC Letter 2014b at 3.

339 CASAC Letter 2014b at 4.
115

xxv. EPA’s Proposal Unlawfully and Arbitrarily 

Discounts and Fails to Protect Against Adverse Effects 

Shown in Epidemiological Studies

As shown above, numerous epidemiological studies show strong associations between a 

variety of serious health impacts and ozone levels well below 70 ppb, including at and below 60 

ppb. In deciding on the level of the standard, however, EPA either disregards or discounts the 

results of most of these studies. In so doing, EPA acted illegally and arbitrarily for the following 

reasons:

1. Except for the panel studies, EPA seems to focus almost entirely on studies published 

after those addressed in the 2006 CD. There is no rational basis for such an approach. 

2. The focus on newer studies results in EPA arbitrarily disregarding or discounting relevant 

evidence. For example, EPA indicates that the only single city epidemiological study showing 

statistically significant associations with adverse effects in an area that would have met the 

current standard is the 2009 Mar and Koenig study, and no single city studies show associations 

in areas that would have a met a standard of 70 ppb or below. See, e.g., 79 Fed. Reg. at 75299/2-

3 (“None of the single-city studies evaluated in section 4.4.1 of the PA...provide evidence for 

O3 health effect associations in locations meeting a standard with a level of 70 ppb or below.” ). 

EPA also asserts that there were no multicity studies for which air quality data indicated that all 

cities included in the analyses would likely have met alternative standard levels. Id. 75307/1-2. 

These assertions ignore: a) the panel studies cited in section 4.4.1 of the PA, which do 

show associations in places where the subjects were exposed to ozone that never exceeded 

various levels below 70 ppb; and b) numerous studies compiled in the last review, and EPA’s 

analysis thereof. As to the latter, Appendix 3B from the Staff Paper in the last review shows a 

number of multi-city and single city studies showing statistically significant associations in 

places that would have met a 98th percentile ozone standard set at various levels below 70 ppb. 

These include: 

 Respiratory Symptoms: Mortimer et al., 2002, 8 U.S. cities (morning symptoms); 

Delfino et al., 2003, San Diego, CA; Ross et al., 2002, East Moline, IL (morning 

symptoms); Ross et al., 2002, East Moline, IL (Evening symptoms)

 Lung Function Changes: Mortimer et al., 2002, 8 U.S. cities (am PEF (%)); Ross et al., 

2002, East Moline, IL PEF (L/min); Brauer et al., 1996, Fraser Valley, BC, FEV1 (mL).

 Emergency Department Visits: Delfino et al., 1997, Montreal (>64yo); Delfino et al, 

1997 Montreal (>64yo); 

 Hospital Admissions: Cardiovascular Diseases: Burnett et al, 1997, Toronto CV.

 Hospital Admissions: Specific Cardiovascular Diseases: Koken et al, 2003, Denver CO, 

myocardial infarction; Koken et al, 2003, Denver CO , Coronary Atheroschlerosis; 

Koken et al, 2003, Denver CO, Pulm Heart Disease.
116

 Hospital Admissions: Respiratory Diseases: Burnett et al, 1997 16 Canadian City; 

Burnett et al, 1997 Toronto; Yang et al., 2003 Vancouver (<3 yo); Yang et al., 2003 

Vancouver (65+ yo).

 Hospital Admissions, Asthma: Burnett et al, 1999, Toronto.

 Hospital Admissions: Other Respiratory Diseases: Burnett et al. 1999, Toronto, 

Respiratory infection

 Mortality: Total nonaccidental: Vedal et al. 2003, Vancouver

3. EPA’s dismissive treatment of the multi-city studies is based on EPA’s view that such 

studies are somehow lacking in probative value unless it is shown that, during the study period, 

all of the cities in the study would have met the 98th percentile form of the ozone standard at 

alternative standard levels under consideration. EPA also asserts that there is greater uncertainty 

in multi-city studies where individual city effect estimates are not presented because it is not 

possible to assign the multicity health effect associations to the air quality in any one study 

location or to the air quality in a particular subset of locations. 79 Fed. Reg. 75307. Neither 

CASAC nor the PA found that the multi-city studies should be discounted on these grounds. 

Although the PA acknowledges there are uncertainties in multi-city studies, it also points out that 

the multi-city studies have advantages in terms of statistical power and number of people and 

variety. Moreover, the PA finds that in four Canadian multicity studies showing positive and 

statistically significant associations between ozone and hospital admissions or mortality, the 

“effect estimates are largely influence by locations meeting the current standard,” suggesting “a 

relatively high degree of confidence in the presence of associations with mortality and morbidity 

for ambient O3 concentrations meeting the current standard.” PA 3-63 to -64. See also PA 3-67. 

The PA further shows that, in two of these studies, the majority of cities would have met a 

standard of 65 ppb. PA. 4-14. The PA concludes that multicity epidemiologic studies report 

positive and statistically significant associations with mortality and morbidity based largely on 

distributions of ambient O3 levels that would have been allowed by alternative standards with 

levels of 70 or 65 ppb, but not 60 ppb. PA 4-17. The PA also finds that cut-point analyses of the 

multicity study by Bell suggests that the large majority of air quality distributions that provided 

the basis for positive and statistically significant associations with mortality (i.e., for the 30 and 

35 ppb cut points) would likely have met the current O3 standard. PA 3-72, -73. 

4. EPA’s discounting of results where the study area would have violated the 98th percentile 

form of a given standard level is arbitrary. As noted by CASAC member Dr. Ana Diez Roux, the 

“ informativeness of these studies depends on the actual distribution and range of ozone 

concentrations investigated rather than on whether the standard was or was not met.” CASAC 

11-26-12 Letter to Administrator at A-12. EPA does not explain why confidence in the 

association of an 8-hour ozone exposure with adverse effects is somehow undermined merely 

because the area in which the association is shown would have violated a 98th percentile form of 

the standard at the same or higher exposure level. EPA does not discount the results of chamber 

studies based on whether the subjects live in areas that would have violated the relevant standard 

levels: There is no rational basis for treating epidemiological studies differently.
117

5. EPA’s dismissive treatment of the multi-city ozone studies in this review in sharp contrast 

to its reliance on such studies for particulate matter See .eg.78 Fed. Reg. 3086, 3150, 3154-55 

(2013). 

2. A Standard Above 60 ppb Cannot Be Justified On This Record

a. EPA Does Not, and Cannot, Show How Any Level Above 60 

ppb Will Protect Sensitive Populations with an Adequate 

Margin of Safety

As described above, exposure to 8-hour average ozone levels of 60 ppb will cause 

adverse effects to sensitive populations. D.C. Circuit case law is clear: “NAAQS must protect 

not only average healthy individuals, but also ‘sensitive citizens’ such as children, and if a 

pollutant adversely affects the health of these sensitive individuals, EPA must strengthen the 

entire national standard.” Coal. of Battery Recyclers Ass’n, 604 F.3d at 618 (internal quotation 

marks and alterations omitted) (quoting American Lung Ass’n, 134 F.3d at 389, and Lead Indus. 

Ass’n, 647 F.2d at 1152-53). Thus, any level above 60 ppb will unlawfully allow adverse effects 

to persist.340

The evidence shows that a level above 60 ppb would not provide any margin of safety for 

sensitive populations. The NAAQS, “as required by the [Clean Air Act],” must “provide an 

adequate margin of safety for vulnerable subpopulations.” Am. Farm Bureau Fed’n, 559 F.3d at 

525-26. A standard that allows adverse effects to persist perforce provides no margin of safety at 

all. At the very least, EPA has failed to explain --in light of the evidence and scientific

recommendations before it—how a standard with a level of 65 to 70 ppb provides an adequate 

margin of safety for sensitive subpopulations.

b. EPA’s Inconsistent Treatment of Adverse Effects is Arbitrary 

and Capricious

EPA irrationally claims that adverse effects have only been demonstrated as low as 72 

ppb, and that it “has less confidence that adverse effects will occur following exposures to O3

concentrations as low as 60 ppb.”341 In particular, EPA relies on chamber studies’ not finding 

“statistically significant increases in respiratory symptoms” below 70 ppb.342 Thus, the agency 

treats lung function decrements as adverse only if combined with respiratory symptoms.343

 

340 Further, as discussed below, the 4th-highest form EPA proposes for the NAAQS would allow up to three 

exposures above 60 ppb to persist every year. Thus, looking at the NAAQS holistically, see Proposed Rule at 

75,305/2 (“the degree of protection provided by any NAAQS is due to the combination of all of the elements of the 

standard”), EPA has not justified why a level above or of 60 ppb, coupled with the 4th-highest form, would protect 

public health. 

341 See, e.g., Proposed Rule at 75,304/3-05/1, 75,309/3.

342 Id. at 75,305/1; see also id. at 75,309/3, 75,310/2.

343 EPA further does not treat the effect as adverse unless the occurrences of both the lung decrements and 

respiratory symptoms are statistically significant, and the respiratory symptoms are statistically significant when 

compared with the symptoms observed under filtered air conditions.
118

This approach conflicts with EPA’s own statements elsewhere in the Proposed Rule. EPA 

itself states that it “considers estimates of the occurrence of O3-induced FEV1 decrements > 10 

and 15 percent as surrogates for the occurrence of adverse health outcomes.”344 EPA and the PA 

further agree that exposure to ozone at 60 ppb causes respiratory effects, including lung function 

decrements that equal or exceed these 10 percent and 15 percent levels.345 EPA itself notes that 

decrements may be adverse in terms of “population risk,” where exposure to air pollution 

increases the risk to the population even though it might not harm lung function to a degree that 

is, on its own, “clinically important” to an individual:

Exposure to air pollution that increases the risk of an adverse effect to the entire 

population is adverse, even though it may not increase the risk of any individual 

to an unacceptable level. For example, a population of asthmatics could have a 

distribution of lung function such that no individual has a level associated with 

clinically important impairment. Exposure to air pollution could shift the 

distribution to lower levels that still do not bring any individual to a level that is 

associated with clinically relevant effects. However, this would be considered to 

be adverse because individuals within the population would have diminished 

reserve function, and therefore would be at increased risk to further environmental 

insult (U.S. EPA, 2013a, p. lxxi; and 75 FR at 35526/2, June 22, 2010).346

Indeed, ozone exposure may make people more susceptible to respiratory infection, allergies, 

and asthma.347 Yet EPA has arbitrarily failed to appropriately consider population risk.

Nor is EPA’s proposed approach to the adversity of lung function decrements consistent 

with EPA’s past practice, ATS guidelines, or CASAC’s advice, which are the only three sources 

of guidance EPA cites in discussing what makes an effect adverse.348 In promulgating a NAAQS 

for SO2 in 2010, EPA explained that, under the 2000 ATS guidelines, “diminished reserve lung 

function in a population that is attributable to air pollution is considered an adverse effect under 

ATS guidance.”349 In promulgating that NAAQS, unlike here, the lung function decrements were 

not statistically significant at the group mean level, yet EPA still found the decrements observed 

there were adverse.350 In the last ozone NAAQS review, EPA itself also acknowledged that a 

lung function decrement of 10 percent or greater “represent[s] a level that should be considered 

adverse for asthmatic individuals.”351 A substantial percentage—at least 10 percent—of healthy,

young adults experience such decrement at 60 ppb,

352 and EPA, CASAC, and the PA all agree 

that at-risk populations, like people with asthma, are likely to experience at least the same 

decrements at the same level of ozone exposure.

353 Finally, CASAC plainly stated that “FEV1

decrement of ≥10 percent is a scientifically relevant surrogate for adverse health outcomes for 

 

344 Proposed Rule at 75,306/1. 

345 Id. at 75,311/2; Policy Assessment at 4-56; see also id.at 75,250-51.

346 Proposed Rule at 75,263/1.

347 Policy Assessment at 3-31.

348 See id. at 75,263/1-64/3

349 75 Fed. Reg. at 35,526/2 (June 22, 2010).

350 Id.

351 73 Fed. Reg. at 16,454/3-55/1 (Mar. 27, 2008).

352 Proposed Rule at 75,250/2 & n.37 (noting that percentage is an underestimate).

353 See, e.g., id. at 75,265/1, /3, 75,280/1 n.92, 75,287/1, 75,288/3, 75295/3, 75,296/2 & n.127.
119

people with asthma and lung disease” and that there are “adverse effects, including clinically 

significant lung function decrements and airway inflammation, after exposures to 60 ppb ozone 

in healthy adults with moderate exertion.”354 Both EPA’s failure to provide any rational 

explanation for its treatment of what makes an effect adverse here and its unexplained departure 

from the sole sources of guidance, as well as its own past finding, it has relied on in the past are 

arbitrary. See American Lung Ass’n, 134 F.3d at 392-93.

EPA’s irrational treatment of the adverse effects observed at 60 ppb is especially 

exacerbated by its departure from both the PA and CASAC’s findings that the effects observed at 

60 ppb are adverse.355 The PA examines population risk and expressly finds that the decrements 

found in the chamber studies at or near 60 ppb fit the ATS criteria for adverse effects.356 As 

described above, CASAC said that the effects at 60 ppb were adverse. EPA thus has failed its 

obligations to confront and explain any departures from CASAC’s advice, and to address 

analyses in the PA that are missing in the Proposed Rule. E.g., Am. Farm Bureau Fed’n, 559 

F.3d at 521 (citing 42 U.S.C. § 7607(d)(3) and NRDC v. EPA, 902 F.2d 962, 967-68, 970 (D.C. 

Cir. 1990), vacated in other part 921 F.2d 326 (D.C. Cir. 1991)).

c. EPA’s Reliance on Its Exposure Risk Assessment to Reject a 

Level of 60 ppb Was Arbitrary and Capricious, Particularly 

Because EPA Is Relying On People Not Going Outdoors to 

Conclude That the Level of Air Pollution Outdoors Will Not 

Harm Them 

As discussed above, section 109 of the Clean Air Act mandates that EPA set the NAAQS 

at a level that allows the public to go out whenever and wherever they want and that the air will 

be clean enough to “protect the public’s health with an adequate margin of safety.” This 

mandate “carries the promise that ambient air in all parts of the country shall have no adverse 

effects upon any American’s health.” 116 Cong. Rec. 42,381 (Dec. 18, 1970) (remarks of 

Senator Muskie, floor manager of the conference agreement). 

Standards must be based on a judgment of a safe air quality level and not on an 

estimate of how many persons will intersect given concentration levels. EPA 

interprets the Clean Air Act as providing citizens the opportunity to pursue their 

normal activities in a healthy environment.

44 Fed. Reg. at 8210. 

In this case, EPA is unlawfully using the HREA to subvert this mandate. EPA is using 

the HREA to justify a level of pollution that is unsafe if actually experienced on the ground that 

people will probably stay indoors. EPA’s rejection of a primary standard of 60 ppb relies 

 

354 CASAC Letter 2014a at 6-7.

355 See, e.g., Policy Assessment at 4-12 (“Thus, 60 ppb is a short-term exposure concentration that may be 

reasonably concluded to elicit adverse effects in at-risk groups”).

356 Id. at 4-52 (“In addition, as discussed in section 3.1.3, such a decrease in mean lung function meets the ATS 

criteria for an adverse response given that a downward shift in the distribution of FEV1 would result in diminished 

reserve function, and therefore would increase risk from further environmental insult.”); see also id. at 4-9, -10. 
120

heavily upon the exposure risk assessment, which concludes that because people will supposedly 

not go outside there will be relatively few “exposures of concern” at this level.357 In other words, 

EPA is relying on people not going outside to set a higher level of ozone that would be unsafe 

when people do in fact go outside: EPA reasons that no one will actually be harmed if they just 

stay indoors.

Even if the EPA’s approach was not completely unlawful—which it is—EPA’s exposure 

risk assessment is itself also technically flawed as it is unable to effectively capture key inputs 

regarding outdoor activity patterns and, as a result, ends up potentially underestimating 

dangerous exposure incidents by sensitive groups such as children and outdoor workers by over 

30 percent.

358

 Furthermore, EPA emphasizes the role of averting behavior, noting that it may 

result in an overestimation of exposures of concern, and cites this behavior (essentially staying 

indoors or not exercising) in order to reach what it deems an acceptable level of risk. But again, 

this is inconsistent with the Clean Air Act’s mandate that EPA set a level that allows people to 

go outside and not put themselves at risk by doing so. What this all means is that first, adequate 

protection of children and others who are active outside, especially during ozone season, is being 

overlooked, and second, the levels of exposure incidents EPA relies on in its decision-making 

may only be reached if people choose not to be active outdoors, but instead stay inside to avoid 

dangerous air pollution.

The Clean Air Act requires that uncertainty be resolved in favor of protecting the public 

health, and that the precautionary principle be applied. Uncertainties in exposure modeling and 

data gaps may be unavoidable, but where they do exist, a precautionary and protective approach 

must be applied. When such uncertainties suggest that it might be unsafe to go outside whenever 

and wherever desired, or “suggest the possibility that some at-risk groups could experience more 

frequent exposures of concern than indicated by estimates made”359, EPA must act in favor of 

protecting sensitive groups.

i. EPA’s Proposed Range of 65 to 70 ppb Undervalues 

Exposure Risk for Children and Outdoor Workers

According to EPA, “the HREA concludes that exposures of concern could be 

underestimated for some individuals who are frequently and routinely active outdoors during the 

warm season,” including “outdoor workers and children who are frequently outdoors.”360

Finding that long-term activity records for such groups do not exist, the HREA notes that 

estimates of high exposures for such groups in the APEX modeling are limited as a result.361 To 

better assess this deficiency, EPA performed limited exposure model sensitivity analyses using 

subsets of activity diaries that were deemed similar to the more active groups. Estimating 

exposures for children who spend large portions of time outdoors during the summer when 

 

357 See e.g., Proposed Rule at 75,297: “Based on the HREA results, meeting an O3 standard with a level of 60 ppb 

would be expected to almost eliminate exposures of concern to O3 concentrations at or above 60 ppb. To the extent 

lower exposure concentrations may result in adverse health effects in some people, a standard level of 60 ppb would 

be expected to also reduce exposures to O3 concentrations below 60 ppb.”

358 Proposed Rule at 75,274.

359 Id.

360 Id. at 75,273 (emphasis added), HREA sec. 5.5. 

361 HREA at 5-78.
121

school is traditionally out of session, EPA found that exposures of concern could be 

underestimated by 33 percent.362 

EPA has estimated that all children in urban areas will experience approximately three 

times more of these “exposures” than adults.363 At the same time, children also experience some 

of the greatest physiological sensitivity to ozone pollution (see section IV.B.1 on children’s 

health). Children spend large amounts of time being physically active outdoors, especially 

during periods (e.g., summers, afternoons) when ozone concentrations are high, and are thus 

more likely to experience dangerous exposures. During the summer, many children spend 

significant amounts of time outdoors and being active at camps and at play. Summertime is also 

when ozone levels are highest, thus putting children at greater risk. 

Every year more than 11 million children, and adults, attend camps in the U.S., not to 

mention over 1.5 million camp workers.364 Most camps last for at least a week, and many for a 

month or two, and over 71 percent of registered camps are overnight camps.365 The majority of 

campers are under age 12366 and the majority of camp activities take place outdoors. According 

to one survey, over 75 percent of both overnight and day camps said campers spent more than 

seven hours a day outside in the open air and only one camp reported less than two hours a day 

spent in the open air.367 Studies of children at summer camps, where they experience sustained 

outdoor activity, show that short-term ozone exposure is associated with decreased respiratory 

function,368 even when restricted for levels above 60 ppb.

369

 Studies of children at summer 

camp with asthma have also shown increased risk of respiratory symptoms on high pollution 

days as well as decreases in lung function.370 

Playing outside and participating in athletics are important parts of a child’s 

development. Over 21 million children play team sports on a regular basis371, although current 

trends show children beginning to spend too much time indoors being inactive.372 Compelling 

children to stay inside to avoid poor air quality and health impacts only further jeopardizes 

 

362 Id. at 5-49; Proposed Rule at 75,274.

363 Proposed Rule at 75,272.

364 American Camp Association, ACA Facts and Trends, available at http://www.acacamps.org/media/aca-factstrends (accessed Mar. 16, 2015).

365 T. Bennett (2014). Fall 2014 Camp Enrollment and Staff Recruitment Survey, American Camp Association, 

available at

http://www.acacamps.org/sites/default/files/images/research/improve/Fall_2014_Enrollment_Survey_Report.pdf.

366 See id. 

367 P.A. James & K.A. Henderson, Camps and Nature Report (2007), available at 

http://www.acacamps.org/sites/default/files/images/research/understand/camps_nature_report.pdf.

368 See e.g., P.L. Kinney, G.D. Thurston, M. & Raizenne (1996). The effects of ambient ozone on lung function in 

children: A reanalysis of six summer camp studies, Env. Health Perspect., 104(2): 170-174; .D. Thurston, M. 

Lippmann, M.B. Scott, & J.M. Fine (1997). Summertime haze air pollution and children with asthma, Am. J. of 

Resp. and Crit. Care Med., 155(2): 654-660. 

369 Spektor, D.M., et al. (1988). Effects of ambient ozone on respiratory function in active, normal children, Am. 

Rev. of Resp. Disease, 137(2): 313-320. 

370 Thurston et al. 1997, supra note 367,

371 The Aspen Institute, Project Play-Facts: Sports Activity and Children, available at 

http://www.aspenprojectplay.org/the-facts.

372 See e.g., id.; Let’s Move, Learn the Facts, available at http://www.letsmove.gov/learn-facts/epidemic-childhoodobesity.
122

healthy lifestyles and development. In one highly significant study, McConnell et al. showed that 

active children who played three or more sports growing up in communities with eight-hour 

ozone levels ranging from 55.8 to a maximum of 69 ppb were three times more likely to develop 

asthma than their peers in communities with lower ozone levels, ranging from 30.6 to 50.9 

ppb.373 Even so, the high pollution communities in the study would uniformly be in attainment 

with EPA’s proposed standard of 70 ppb—meaning that EPA’s proposed standard of 70 ppb 

would do nothing to address these exposures and the associated health impacts. The authors 

found that “new diagnoses of asthma is associated with heavy exercise in communities with high 

concentrations of ozone, thus, air pollution and outdoor exercise could contribute to the 

development of asthma in children.”374

Indeed, even a cursory review of camp programs in the United States makes evident just 

how many camps emphasize extended outdoor time for children. As is evident in the 

advertisements for these camps included in Exhibit 7 many of these camps focus on extensive 

outdoor exercise and sports, including baseball, basketball, football, soccer, field hockey, tennis, 

swimming, canoeing, kayaking, hiking, and ropes courses. And they cater to a wide age range of 

children from five and six years old through the teen years. These are precisely the types of 

conditions that lead to maximum exposure—extended outdoor time, with heavy exercise and 

ventilation—for one what the scientific literature demonstrates is a highly sensitive population. 

Children who are active outdoors aren’t the only ones at special risk, although children 

are particularly vulnerable to the health impacts of ozone exposure due to their life stage and 

physiological factors. Even healthy adults who are active outdoors face greater exposure and 

health risks. In one study by Kinney and Lippmann of 72 sophomore cadets from the U.S. 

Military Academy at West Point during summer training demonstrated a seasonal decline in 

respiratory function when outdoors in the presence of ozone.375 Similarly, a study of outdoor 

farm workers in British Columbia found associations between ozone concentrations and 

decreases lung function that persisted at mean daily maximum 1-hour ozone concentrations of 

less than 40 ppb.

376

 Another study of healthy, adult, amateur cyclists found ozone associations to 

be associated with decreases in lung function and increases in respiratory symptoms, even at 8-

hour ambient concentrations of less than 60 ppb.

377

The HREA is also missing activity profiles from outdoor workers, so EPA performed an 

assessment to estimate what exposures of concern might look like for this group. EPA calculated 

that approximately 30 percent of outdoor workers, who aren’t adequately accounted for in the 

exposure modeling, would experience at least one exposure of concern over 60 ppb, compared to 

5 to 8 percent of the general population of workers.378 These results “suggest the possibility that 

 

373 R. McConnell et al. (2002). Asthma in exercising children exposed to ozone: A cohort study, Lancet, 359(9304): 

386-391. 

374 Id. 

375 P.L. Kinney. & M.Lippmann, Respiratory effects of seasonal exposures to ozone and particles, Arch. of Env. 

Health,, 55(3), 210-216 (2000).

376 M. Brauer, J. Blair, & S. Vedal (1996). Effect of ambient ozone exposure on lung function in farm workers, Am. 

J. of Resp. and Crit. Care Med., 154(4): 981-987.

377 B. Brunekreef et al. (1994). Respiratory effects of low-level photochemical air pollution in amateur cyclists, Am. 

J. of Resp. and Crit. Care Med., 150(4): 962-966.

378 HREA at 5-51.
123

some at-risk groups could experience more frequent exposures of concern than indicated by 

estimates made using the full database of activity diary profiles.”379

It should also be noted that exposures may at the same time be underestimated for all 

groups due to the use of the maximum 8-hour average metric. EPA comments that “that it is 

entirely possible multiple benchmark exceedances could occur for an individual on certain high 

ambient O3 concentration days” but that “this is not a practical output for the purposes of this 

assessment.”380

ii. EPA Impermissibly Relies on People Staying Indoors to 

Avoid Repeated or Prolonged Exposure to the Air

At the same time, EPA suggests that exposures are probably overestimated due to people 

staying indoors.381 In evaluating alternative primary standards, EPA repeatedly emphasizes the 

HREA modeling and quantitative exposure assessment, though EPA questions whether the 

exposure assessment may overestimate exposures, due to people staying indoors to avoid poor 

air quality, while also underestimating critical exposures for children and others who are active 

outdoors. EPA suggests that behavioral changes to stay indoors and reduce exposure to poor air 

quality can “reduce the percentages of children estimated to experience exposures of concern at 

or above the 60 or 70 ppb benchmark concentrations by approximately 10 to 30 percent, with 

larger reductions possible for the 80 ppb benchmark.”382 The HREA modeling of averting 

behavior showed that 15.3 percent of schoolchildren in Detroit spent on average 44 minutes less 

time outdoors –“resulting in approximately one percentage point or fewer children experienced 

exposures at or above any of the selected benchmark levels.”383 For asthmatic schoolchildren, 

this resulted in 20.3 percent spending on average 44 minutes less time outdoors and resulted in 

approximately two percentage points or fewer experienced exposures at or above any of the 

selected benchmark levels.384

Although, in the HREA, EPA recognizes evidence that many people, including children, 

avert outdoor activity and that the exposure estimates may be too high due to averting behavior, 

it is also unclear whether there is double-counting of the impact of averting behavior. In a 

footnote, EPA notes that “we do not know if any diary day represents the activities of an 

individual who averted. Thus it is entirely possible that the ‘no averting’ simulation includes, to 

an unknown extent, individuals who spent less time outdoors than would have occurred if 

absolutely no individuals averted.”385 In other words, EPA does not know if the activity data it is 

using already includes double-counting averting behavior, but chooses to assume it does not in 

their basis for calculating exposures of concern and, consequently, reduces its estimates of risks. 

In order to reach what EPA unlawfully and irrationally concludes is justifiably low risk, EPA is 

discounting the number of events of unsafe air based upon EPA’s deeply flawed—and 

unlawful—analysis that people will for one reason or another not be outside and thus will not be 

 

379 Proposed Rule at 75,274.

380 HREA at 5-18.

381

 See Proposed Rule at 75,276.

382 Proposed Rule at 75,274; HREA Fig. 5–15.

383 HREA at 5-53.

384 HREA at 5-53 – 5-54.

385 HREA at 5-53, n. 27.
124

exposed to the unsafe levels of ozone that EPA is proposing to allow. Putting aside the unlawful 

nature of EPA’s approach, from a purely technical assessment, EPA cannot rely on averting 

behavior as a measure to lower risk and exposures of concern because it cannot accurately gauge 

the extent of averting behavior based on the data it has. 

EPA’s discussion of averting behavior inappropriately, unethically, and unlawfully 

amounts to advocating for it, and cannot provide an option for protecting public health: 

“Individuals can reduce their exposure to O3 by altering their behaviors, such as by staying 

indoors, being active outdoors when air quality is better, and by reducing their activity levels or 

reducing the time being active outdoors on high-O3 days.”386 EPA’s observation that “the results 

suggest that exposures of concern could be overestimated, particularly in children, if the 

possibility for averting behavior is not incorporated into estimates” unlawfully and arbitrarily 

promotes a standard that would effectively compel sensitive populations to remain indoors.387 

iii. The Sufficiency of the NAAQS to Protect Public Health 

Cannot Depend upon Sensitive Populations Remaining 

Indoors

Air quality standards cannot rely on avoidance behavior in order to protect the public 

health and sensitive groups. The promise of the Clean Air Act is to clean up the air so that 

anyone can go outside anytime and the air will be safe to breathe, and that assessment of safety 

will be based on the best assessment of up-to-date science. Thus, meeting the NAAQS does not 

mean that the air is only safe to breathe part of the time. It would be unlawful for EPA to set the 

standard at a level that is contingent upon people spending most of their time indoors.

Not only is it unlawful to set the standard based on an expectation that people will spend 

most of their time indoors, but such an approach carries serious consequences for public health. 

There are significant health benefits to be gained by spending time outdoors. Forcing sensitive 

groups to stay indoors in order to avoid unhealthy air quality levels puts them in a position of 

either avoiding outdoor activity, thus raising the risk of obesity and other health problems, or 

going outside and running the risk of respiratory disease and asthma attacks. Unfortunately, 

some opponents of a more protective ozone standard have already argued that staying indoors is 

an acceptable protection. EPA cannot base its final decision on any aspect of assumed avoidance 

of exposure.

EPA is effectively discouraging the very types of healthy exercise and outdoor behaviors 

that we want to be encouraging and that are in such critical jeopardy in this country. In recent 

years, childhood obesity has skyrocketed in the U.S., more than doubling for children and 

quadrupling for adolescents over the past three decades.388 In 2012, over one third of children 

and adolescents were either overweight or obese, putting them at greater risk for cardiovascular 

disease, diabetes, bone and joint problems, social and psychological problems, and even cancer 

 

386 Proposed Rule at 75,269.

387 Proposed Rule at 75,274.

388 CDC, Childhood Obesity Facts, available at http://www.cdc.gov/healthyyouth/obesity/facts.htm; see also Let’s 

Move, supra note 371. 

388 CDC, Childhood Obesity Facts, available at http://www.cdc.gov/healthyyouth/obesity/facts.htm
125

in the long-term.389

Outdoor activities and spending time in natural environments can help combat the rise of 

health conditions such as obesity, type 2 diabetes, vitamin D deficiency, and attentiondeficit/hyperactivity disorder (ADHD), all of which sedentary indoor lifestyles contribute to.390

Research shows that both physical activity and exposure to nature promote good physical and 

mental health and well-being, especially for children.391 Time spent outdoors is associated with 

higher levels of physical activity.392 Children who spend more time outside not only tend to be 

more physically active, but are also less likely to be overweight.393 Furthermore, in addition to 

increasing physical activity and health, time spent outdoors is shown to improve children’s sense 

of well-being and feelings of health, safety, and satisfaction.394 Time spent outside has cognitive 

benefits and can help decrease childhood stress, improve attention, and reduce the symptoms of 

ADHD.395 Physical activity and contact with nature are also beneficial to psychological wellbeing, leading to improvements in self-esteem, depression and mood.396

Instead of encouraging active, healthy lifestyles, EPA proposed range of 65 to 70 ppb

would result in levels of air quality that force people inside. Additional health benefits provided 

by standards of 65 or 70 ppb are undermined to the extent they depend on lifestyle changes that 

increase other health risks. The purpose of the Clean Air Act is “to protect and enhance the 

quality of the Nation’s air resources as to promote the public health and welfare and the 

productive capacity of its population.” 42 U.S.C. § 7401(b)(1). As such, it is unacceptable for 

EPA to rely on people staying indoors in order to deem the level of risk satisfactorily low. 

Everyone has the right to go outside—and to not experience health risks when doing so. 

 

389

 Id. 

390 L.E. McCurdy, K.E. Winterbottom, S.S. Mehta, & J.R. Roberts (2010). Using nature and outdoor activity to 

improve children's health, Current Problems in Pediatric and Adolescent Health Care, 40(5): 102-117.

391 G. Godbey (2009). Outdoor Recreation, Health, and Wellness: Understanding and Enhancing the Relationship, 

Resources for the Future; J. Pretty et al. (2009). Nature, Childhood, Health and Life Pathways. Interdisciplinary 

Centre for Environment and Society Occasional Paper 2009-02; S.A. Muñoz (2009). Children in the outdoors: a 

literature review, Sustainable Development Research Centre.

392 A.R. Cooper et al. (2010). Patterns of GPS measured time outdoors after school and objective physical activity in 

English children: the PEACH projec, Int. J. of Behavioral Nutrition and Phys. Activity, 7(31); A. Nilsson et al. 

(2009). Correlates of objectively assessed physical activity and sedentary time in children: a cross-sectional study, 

BMC Public Health, 9(322); T. Hinkley, D. Crawford, J. Salmon, A.D. Okely, & K. Hesketh (2008). Preschool 

children and physical activity - A review of correlates, Am. J. of Prev. Med., 34(5): 435-441; J. Sallis, J. Prochaska, 

& and W. Taylor (2000). A Review of Correlate of Physical Activity of Children and Adolescents, Med. and 

Science in Sports and Exercise, 32(5): 963–75.

393 V. Clelandet al. (2008). A prospective examination of children's time spent outdoors, objectively measured 

physical activity and overweight, Intl.. J. of Obesity, 32(11):1685-1693.

394 C. Wood, R. Hine, & J. Barton (2011). The health benefits of the Youth Outdoor Experience (YOE) project: 

University of Essex. 

395 McCurdy et al. 2010, supra note 326.; M.G. Berman, J. Jonides, & S. Kaplan, The Cognitive Benefits of 

Interacting With Nature. Psychological Science, 19(12),. 1207-1212 (2008); N.M. Wells, At Home with Nature: 

Effects of “Greenness” on Children’s Cognitive Functioning, Environment and Behavior, 32(6), 775-795 (2004); F. 

Kuo. & A. Taylor, A,A Potential Natural Treatment for Attention-Deficit/Hyperactivity Disorder: Evidence from a 

National Study, Am. J. of Public Health, 94(9), 1580–86 (2004); Godbey 2009, supra note 390.

396 Wood et al. 2011, supra note 393. 
126

d. EPA’s Risk and Exposure Assessment Has Substantial 

Limitations that Severely Underestimate the Health Impacts of 

Exposure

EPA’s quantitative HREA is intended to elucidate the potential public health implications 

of current and proposed alternative standards. With any such analysis, multiple analytical 

assumptions can greatly affect the result and multiple uncertainties can diminish the reliability of 

those results. The selection of factors such as risk coefficients used, health impacts analyzed, 

years of air quality monitoring utilized, exposure assumptions, and other variables can have a big 

impact on the outcomes. Although the HREA clearly demonstrates three key aspects: the burden 

that current concentrations of ozone pose to public health; the inadequacy of the current standard 

of 75 ppb to provide the legally required protection; and the evidence that the lower the standard, 

the greater the reductions in exposure and risk that could be achieved. However, several factors 

and limitations in the scope of the risk assessment result in severe underestimates of exposures of 

concern and of health impacts. 

i. Infants and Small Children Are Excluded

First, children aged zero to five are among the most susceptible populations, but they are 

not included in the quantitative risk and exposure assessment examining lung function 

decrements in children. This is a serious omission. Approximately 20 million children in the U.S. 

fall within the 0-5 age group, yet they are completely disregarded in the risk estimates. 

We know that the lungs are not fully developed at birth, and that ozone exposure can 

affect the post-natal development of the lungs. Infants are exposed to outdoor air at an early age 

and they are active outdoors from the time they are mobile. They experience higher exposures 

than adults because of their increased breathing rate and activity level. By excluding infants and 

young children from the analysis, EPA greatly underestimates exposures of concern and risks. 

ii. A Very Narrow Subset of Health Endpoints are 

Evaluated 

Second, the health endpoints considered in the REA are extremely limited, and do not 

represent the comprehensive array of health effects attributable to ozone exposure. For instance, 

the analysis mainly looks at lung function decrements, respiratory hospitalizations, and mortality. 

Respiratory emergency room visits are considered in only two cities, and respiratory symptoms 

in only one city. Because of the quantitative nature of the results, the available effect estimates 

are emphasized in the proposal, to the exclusion of the vast array of other health endpoints of 

concern. As a result, EPA understates risks.

iii. Exposures of Concern are Evaluated for Limited 

Scenarios

Third, the analysis only considers alternative levels the standard of 70, 65, and 60 ppb. 

At 60 ppb, we know that healthy adults experience lung function declines and inflammation with 

6.6 hour exposures. Children and those with respiratory disease are considered sensitive 
127

populations and would likely experience effects at lower concentrations. Further, the risk 

function is based on a 6.6 hour exposure, whereas the standards are based on 8 hours. For these 

reasons, by failing to consider exposures of concern of 55 ppb, the exposure assessment 

underestimates risks. 

iv. A Risk Function Derived from Study of Healthy Adults 

Is Inappropriately Applied to Children

The HREA uses a risk function derived from a controlled human exposure study of 

healthy young adults to estimate lung function decrements in children, including children with 

asthma. This assumption could result in an underestimate of risk. 

v. The Geographic Scope of the Analysis is Limited

The HREA is too limited in its geographic scope. Respiratory admissions are estimated 

for only one city, Boston. Respiratory function declines are estimated for only 15 cities (and 

only 14 cities for the 60 ppb standard level, e.g., 79 Fed. Reg. at 75,297 n.135), and respiratory 

emergency department visits are assessed for 2 cities, Atlanta and New York. Mortality 

estimates are made for just 12 cities. Effects on rural populations are not estimated, even though 

some rural areas experience higher ozone concentrations than urban areas. 

vi. EPA Looks at Just Two 3-Year Periods to Estimate Air 

Quality 

The EPA analysis uses air quality data from two 3-year periods: 2006 to 2008; and 2008 

to 2010. The results for these two periods vary considerably, depending on which time frame 

had better air quality. The proposal presents results from an average of these two periods. From 

a standpoint of evaluating public health protection, it is more appropriate to place greater weight 

on the years with poorer air quality. 

vii. The Emission Control Strategies Modeled Are Limited 

Finally, it should be emphasized that the emissions control strategies modeled in the draft 

HREA are limited. Localities will consider many additional factors such as updated emissions 

inventories and a variety of NOx and VOC control measures that were not analyzed in the risk 

assessment. By focusing on NOx reductions, the risk assessment results are distorted for some 

areas of the country.

e. Despite These Limitations, the Health Risk and Exposure 

Assessment and Regulatory Impact Analysis Support Setting 

the Standard at 60 ppb

As described elsewhere in these comments, EPA misuses the HREA to try to justify a 

weaker standard. Yet that document, even with its underestimates of exposures and health 

effects, actually undercuts EPA’s efforts. So too does the Regulatory Impact Assessment, where 
128

it estimates the health benefits resulting from different levels of the standard. What follows is a 

sampling of data derived from those documents. More supportive data can be found in them.

Controlled human exposure studies have shown, as discussed elsewhere, that exposure to 

60 ppb of ozone over a 6.6 hour period causes adverse effects in healthy adults. Sensitive 

subjects, like children, asthmatics, and seniors, are more vulnerable. Table 6and figure Y1 below 

demonstrate not only that the current standard is much weaker than required, but also that only a 

standard of 60 ppb brings the occurrence of these dangerous exposures to anywhere approaching 

zero—which is what the Clean Air Act demands.

TABLE 6 Mean number of people with at least one daily maximum 8-hr average O3 

Exposure at or above 60ppb while at moderate or greater exertion (includes 15 urban area 

studies)

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for Ozone: Final Report 5-87 

tbl.5-13 (August 2014). 

Standard 8-hr 

level

School age 

children

Asthmatic 

school-age 

children

Asthmatic adults Seniors (aged 

65-95)

60 ppb 70,000 7,700 4,100 6,800

65 ppb 392,000 42,000 25,000 38,000

70 ppb 1,176,000 126,000 83,000 129,000

75 ppb 2,316,000 246,000 180,000 282,000

FIGURE 6 Increased Exposure for At-Risk Groups According to Ozone Standard (with at 

least one daily 8-hr average O3 exposure at or above 60ppb while at moderate or greater 

exertion)

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for Ozone: Final Report 5-87 

tbl.5-13 (August 2014). 

0

500,000

1,000,000

1,500,000

2,000,000

2,500,000

Persons

exposed at 60

ppb

Persons

exposed at 65

ppb

Persons

Exposed at 70

ppb

Persons

exposed at 75

ppb

school age children

asthmatic school age children

Seniors

asthmatic adults
129

Similarly, Tables 7 and 8 and Figures 7 and 8 below show that a standard of 60 ppb is 

necessary to truly reduce occurrence of adverse lung function decrements in children to levels 

near what the Clean Air Act calls for. 

TABLE 7 Maximum Percentage Children (ages 5-18) Experiencing Decreased Lung 

Function According to Ozone Level (During the O3 Season) 

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for Ozone: Final Report 6-22 

to -27 tbls.6-4, 6-5 (August 2014). 

Standard

Percent of Children 

Experiencing 1 Day 

or More of Lung 

Function Decrement 

≥10%

Percent of Children 

Experiencing 1 Day 

or More of Lung 

Function Decrement 

≥ 15%

Percent of Children 

Experiencing 6 Days 

or More of Lung 

Function Decrement 

≥10%

60 ppb 13% 3% 3%

65 ppb 18% 4% 4%

70 ppb 20% 5% 5%

75 ppb 22% 6% 6%

FIGURE 7 Increase in Maximum Percentage of Children (ages 5-18) to Experience Lung 

Function Decrement Arranged According to Alternate Ozone Standards

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for Ozone: Final Report 6-22 

to -27 tbls.6-4, 6-5 (August 2014). 

TABLE 8 Lung Function Decrements for Alternate Ozone Standards for Children (ages 5-

18) Experiencing One or More Decrements Per Season

(Data derived from 79 Fed. Reg. at 75,298 tbl.5) 

0% 5% 10% 15% 20% 25%

70 ppb

65 ppb

60 ppb

Children Experiencing Lung

Function Decrement of 10% or

greater for 6 days or more

Children Experiencing Lung

Function Decrement of 15% or

greater (1 day or more)

Children Experiencing 1 Day or

More of Lung Function

Decrement 10% or greater
130

Decreased Lung 

Function

Alternate Ozone 

Standard

Number of children 

experiencing 

decrement

Average % reduction 

from current standard

≥10% 60 ppb 1,404,000 45%

65 ppb 1,896,000 31%

70 ppb 2,527,000 15%

≥15% 60 ppb 225,000 67%

65 ppb 356,000 50%

70 ppb 562,000 26%

≥20% 60 ppb 57,000 77%

65 ppb 106,000 59%

70 ppb 189,000 32%

FIGURE 8

Percent reductions in each urban study area were calculated and averaged across areas 

(excluding NY for 60ppb) (Data derived from 79 Fed. Reg. at 75,297-98 tbl.4)

In the Proposed Rule, EPA declines to highlight the benefits of more protective standards 

for outdoor workers, who form another sensitive population. As summarized in Figure 9 below, 

EPA’s quantitative assessment of those benefits again demonstrates the virtue of the 60 ppb 

standard, both for outdoor workers and the general population, in terms of preventing lung 

function decrements of ≥15%.

FIGURE 9 Percentage of Outdoor Workers (age 19-35) Experiencing One or More Lung 

Function Decrement of at least 15%

0% 20% 40% 60% 80% 100%

≥ 10%

≥ 15%

≥ 20%

70 ppb

65 ppb

60 ppb

Lung 

function 

decrement

Percent reduction by 

ozone alternate 

standard 
131

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for 

Ozone: Final Report 6-29 tbl.6-6 (August 2014).) 

A more protective ozone standard would also prevent deaths from long-term ozone 

exposure. Figure 10 below compares how many lives would be saved at a 60 ppb level (over the 

current standard of 75 ppb) against the numbers saved at 65 ppb and 70 ppb (both also over the 

current standard) in just a few of the cities EPA assessed. This shows that a 70 ppb standard 

would have only a slight effect, and a 60 ppb standard would be many times more effective.

FIGURE 10 Long-term Respiratory Mortality in Certain Cities attributed to Ozone based 

on 2009 Air Quality Data

(Data derived from EPA, EPA-452/R-14-004a, Health Risk and Exposure Assessment for 

Ozone: Final Report 7-62 tbl.7-12 (August 2014)) 

0.00% 1.00% 2.00% 3.00% 4.00% 5.00%

existing standard

70 ppb

65 ppb

60 ppb

Outdoor Workers

General Population
132

In the Regulatory Impact Analysis, EPA modeled a broader range of health benefits 

resulting from more protective ozone standards. These data allow calculations of the benefits—

shown in Table 9 and Figure 11 below—foregone by establishing unlawfully and irrationally 

under-protective standards, as opposed to a 60 ppb standard. These show that a 60 ppb standard 

would reap more than twice the benefits of a 65 ppb standard, compared to a 70 ppb standard. 

EPA must set the level at 60 ppb.

TABLE 9 Yearly Death and Morbidity Rates According to Ozone Standards: 2025 National 

Benefits (except California)

(Data derived from EPA, EPA-452/P-14-006, Regulatory Impact Analysis of the Proposed Revisions to the National 

Ambient Air Quality Standards for Ground-Level Ozone at ES-14 to -15 tbl.ES-7 (November 2014))

Alternative Standard Levels

60ppb versus 

70ppb: Additional 

persons protected

60 ppb versus 65 

ppb: Additional 

persons protected

65ppb versus 70ppb: 

additional persons 

protected:

Short-term exposure 

related premature 

deaths avoided*

1560 900 660

Long-term exposurerelated premature 

deaths avoided (age 

30+)

3220 1800 1420

0

20

40

60

80

100

120

Atlanta Boston Philadelphia Houston, TX

75-70ppb

75-65ppb

75-60ppb

Change in 

ozone attributed 

mortality based 

on alternate 

standards:
133

Non-fatal heart 

attacks (18-99)*

2500 1400 1100

Respiratory Hospital 

Admissions (age 0-

99)

2390 1400 990

Cardiovascular 

hospital admissions 

(age 8-99)

770 420 350

Asthma emergency 

department visits 

(age 0-99) 

6600 3700 2900

Acute bronchitis 

(age 8-12/3rd to 7th

grade children)

3310 1800 1510

Asthma exacerbation 

(age 6-18)

1,480,000 840,000 640,000

Lost Work Days 

(age 18-65)

275,000 160,000 115,000 

Minor restricted 

activity days (age 

18-65)

6,000,000 3,300,000 2,700,000

Upper & lower 

respiratory 

symptoms (children 

7-14)

106,000 60,000 46,000

School loss days 

(ages 5-

17/kindergarten to 

12th grade

1,570,000 900,000 670,000

*Maximum amount avoided death or morbidity rates found for each alternative standard used as 

a basis for comparison.

FIGURE 11 Increase in Deaths and Asthma-Induced Trips to the Emergency Room

Between Alternate Ozone Standards. 

(Data derived from EPA, EPA-452/P-14-006, Regulatory Impact Analysis of the Proposed Revisions to the National 

Ambient Air Quality Standards for Ground-Level Ozone at ES-14 to -15 tbl.ES-7 (November 2014)) 
134

3. EPA Proposes a Form of the NAAQS-- the Fourth Highest 8-hour 

Maximum Averaged Over 3 Years--That Will Fail to Deliver the 

Public Health Protection that EPA Itself Ultimately Concludes is 

Necessary; Whatever Nominal Level EPA Adopts, the Form Will 

Allow Repeated Exceedances of the Standard Each Season Without 

Triggering a Nonattainment Designation or Any Obligation to Clean 

up the Air and EPA Must Compensate For This By Setting An 

Accordingly Lower Nominal Level Of The Standard 

In light of the form of the standard proposed, EPA’s basis for rejecting a level of 60 ppb 

and instead proposing a level in the range of 65 to 70 ppb is based on a flawed characterization 

of the relationship between the level of the standard and actual occurrences of ozone levels in the 

ambient air. EPA purports to reject a standard of 60 ppb on the basis that it “would place a large 

amount of weight on the potential public health importance of virtually eliminating even single 

occurrences of exposures of concern at and above 60 ppb.”397 Instead “the Administrator 

focuses on the extent to which a revised standard would be expected to protect populations from 

experiencing two or more O3 exposures of concern (i.e., as a surrogate for repeated 

exposures).”398 Yet given the proposed form of the standard—the 3-year average of 4th high 

daily maximum 8-hour ozone values—the standard is far less protective of human health than its 

nominal level suggests. Indeed a standard with a nominal level of 65 or 70 ppb would expressly 

authorize numerous occurrences of and exposures to 8 or more hours to levels in excess of these 

levels each year without triggering a nonattainment designation or other ameliorative 

requirements under the Clean Air Act and requirements to clean the air. Given EPA’s 

 

397 Proposed Rule at 75,309. 

398 Id. at 75,305. 

0

1000

2000

3000

4000

5000

6000

7000

Additional Deaths from long

term exposure

Additional asthma

emergency department

visits

Due to using 70 ppb instead of

60 ppb standard

Due to using 65 ppb instead of

60 ppb
135

recognition that even single exposures399—and certainly multiple exposures400—to levels of 70 

ppb are potentially adverse, a standard of 70 ppb unlawfully fails to protect the public from 

acknowledged adverse effects. Likewise, empirical data show that a standard of 65 ppb would 

allow numerous exposures of concern each year. Because multiple 8 hour occurrences of air 

quality levels above the NAAQS will regularly occur in areas meeting the 4th high form of the 

standard, a lower level of the NAAQS is required to achieve EPA’s claimed level of health 

protection. 

a. Multiple Aspects of the NAAQS Define the Stringency of the 

Standard

Several elements define each National Ambient Air Quality Standard. The standard has a 

form, an averaging time, an indicator, and a level. Each of these elements, as well as other 

factors such as monitoring regime affects the stringency of the standard. For example, EPA’s 

original primary NAAQS for photochemical oxidants established in 1971 differed from the 

current and proposed standard in several of the elements, which rendered the 1971 standard

significantly more health protective. While the level of the original 1971 NAAQS—0.08 ppm—

was slightly higher than the current 0.075 ppm level, each of the other elements worked together 

to make the standard far more protective of health. Rather than using ozone only as an 

indicator, the 1971 standard used total photochemical oxidants, a broader category of pollutants 

and thus one that occurs in higher concentrations than ozone alone. Rather than using an 8-hour 

averaging time, the 1971 standard employed a 1-hour averaging time. And rather than rely on a 

statistical form that considers the 4th high 8-hour daily max averaged over three years, the 1971 

standard used a deterministic “not to be exceeded more than one hour per year” form. Taken 

together, the four elements of the 1971 NAAQS rendered it far stronger than the 2008 standard

now in effect. 

EPA’s proposed revision of the standard is flawed because it attempts to divorce its 

analysis of each of the elements of the standard and consider each in isolation. Thus, EPA 

discusses the scientific research on ozone in the context of the level of the standard only. But 

every element of the form that EPA has proposed then renders the nominal numerical level far

less protective than—and further divorced from—the underlying science. Thus EPA’s attempt to 

bestow the imprimatur of CASAC approval on its election to use the 4th high 8-hour daily max 

form is deeply problematic. CASAC supported the form as part of a complete standard with 

level, indicator, and averaging time. Altering any one of these elements changes the overall 

protectiveness of the standard. Selecting a 4th high 8-hour daily max form necessitates that EPA 

recognize that it is far less protective than a deterministic 1st high or even a three-year average 1st

high 8-hour daily max form. 

 

399 In the proposed rule EPA acknowledges that “single exposures of concern could be adverse for some people, 

particularly for the higher benchmark concentrations (70, 80 ppb) where there is stronger evidence for the 

occurrence of adverse effects.” Id. at 75,289. 

400 EPA acknowledges moderate lung function decrements at 70 ppb. And EPA acknowledges that “Thus it has 

been judged that repeated occurrences of moderate responses, even in otherwise healthy individuals, may be 

considered to be adverse since they could well set the stage for more serious illness.” Id. at 75,264. 
136

Stated another way, if EPA wants to ensure that people in fact are not exposed to levels 

of 70 ppb for 8 hours more than once, and yet EPA wants to use the proposed form of the 4th

highest averaged over three years—which dismisses the first three occurrences each year—EPA 

will have to set the nominal numerical standard far below 70 ppb. Indeed, as discussed below, 

empirical data from the last 13 years shows a very consistent pattern: the 1st high averaged over 

three years is approximately 7.6 ppb higher than the 4th high, the second high is approximately 

3.8 ppb over the 4th high. As a result, if EPA adopts the form it has proposed, a nominal level of 

70 ppb is actually equivalent to a level of approximately 78 ppb, which is clearly far in excess of 

what all the science, and EPA itself, says is a safe level of the NAAQS. However, as discussed 

below, each element of the form adds a further weakening the standard.

b. EPA’s Proposed Form and Averaging Time of the NAAQS 

Requires that the Level of the Standard be Lowered to Achieve 

EPA’s Claimed Level of Health Protection. 

i. An 8-hour Averaging Time is Longer than the 

Controlled Human Exposure Studies Relied upon by 

EPA; Extrapolating the Results of These Studies to 8 

Hours Would Produce Larger and More Pervasive 

Impacts to Test Subjects, Necessitating a Lower Level 

of the NAAQS. 

Despite discussing at length the controlled human exposure studies identifying 

acknowledged adverse effects (combination of lung function decrements and symptoms) at 72 

ppb based on exposures in healthy individuals for 6.6 hours, EPA proposes a form of the 

standard with a longer averaging time than the studies it bases its analysis on. Ozone levels that

EPA identifies as being of concern based on exposures of 6.6 hours will pose even greater threats 

to health under longer 8-hour exposures. Indeed, as discussed above, it is well established by 

now that there is a dose response curve to ozone. In order to protect public health with an 

adequate margin of safety, EPA cannot simply treat the results of human controlled studies based 

on 6.6- hour exposures as determinative of impacts based upon 8-hour exposures. Indeed, an 8 

hour exposure period will result in a 21 % increase in exposure time over the 6.6 exposures in 

the clinical trials. Stated another way, if EPA sets a level of 70 ppb, but uses an 8-hour exposure 

timeframe instead of the 6.6 hour timeframe used in the controlled human exposure studies that 

underpin EPA’s standard, EPA must first identify the effect that that has on overall dose 

response outcomes and account for it in setting the nominal numerical level of the standard. 

Simply put, if EPA is going to increase dose time, it needs to understand the effects of doing so 

and then build additional protection into the standard by adopting a level that accounts for the 

less protective form and averaging time of the proposed standard. 

Moreover, the form of the standard considers ozone levels only during one 8-hour period 

each day. Elevated ozone concentrations outside this peak period are wholly disregarded under 

the proposed form of the standard. Unsafe ozone levels could occur for 24 straight hours on one 

day at average levels above the NAAQS and yet that day would be treated no differently from a 

day during which elevated ozone concentrations were limited to a period of only eight hours. 
137

In using an 8-hour averaging time while relying on scientific studies with exposure times 

of only 6.6 hours, EPA must adjust the level of the standard downward from what the scientific 

studies directly concluded in order to account for the longer averaging time of the proposed 

standard. 

ii. Because of EPA’s Truncating Conventions, Any Ozone 

Standard Proposed is, as a Practical Matter, a Full Part 

Per Billion Higher; EPA Must Account for this UnderProtection in Setting the Level of the Standard

EPA’s truncating conventions result in almost a full part per billion of under-protection in 

the level of the NAAQS that needs to be accounted for when setting the new standard. EPA 

assiduously documents throughout its proposal that the Schelegle et al. study identifying adverse 

effects in healthy individuals at “70 ppb” actually had an average exposure concentration of 72 

ppb, attempting to draw a meaningful distinction between levels of 72 and 70 ppb. But EPA 

fails to acknowledge anywhere in its proposal that because of its truncating conventions, an area 

can have 8-hour daily maximum ozone levels and design values almost a full part per billion in 

excess of the level of the NAAQS without triggering a nonattainment designation. That is, built 

into EPA’s calculation of design values is a full part per billion of under-protection because both 

8-hour daily maximum concentrations and 3-year averages of 4th highest maximum 8-hour 

average concentrations are recorded in parts per million and truncated after the third decimal 

digit.401 The practical consequence is that a standard of 70 ppb is effectively a standard of 71 

ppb and a standard of 65 ppb is effectively a standard of 66 ppb. EPA must take into account 

this under-protectiveness by setting the level of the standard one part per billion lower than 

would otherwise be required by the science.

iii. Because of the Real-World Relationship Between the 3-

Year Average of 1st, 2nd and 4th Highest 8-hour Daily 

Monitored Maximum Ozone Concentrations, Use of a 

4

th Highest Form Is Equivalent to Use of a 1st Highest

Form with a Level 7.5 to 8 ppb Higher and to a 2nd

Highest Form with a Level 3.5 to 4 ppb higher; EPA 

Must Account for this Under-Protection in Setting the 

Level of the Standard

EPA must reconcile its choice of a 4th highest form for the proposed standard with its 

identified concerns regarding single and multiple exposures to elevated levels of ozone. Even 

 

401 See id. at 75,352 ("The EPA is proposing to maintain the requirement that hourly O3 concentration data be 

reported in parts per million (ppm) to three decimal places. Any decimal digits reported beyond three decimal digits 

will be truncated, consistent with past practice (40 CFR part 50, Appendix P, section 2.1) and the typical 

measurement uncertainty associated with most O3 monitoring instruments."); see also 73 Fed. Reg. 16,501 (Mar. 

21, 2012) ("Consistent with the current approach for computing 8-hour averages, in calculating 8-hour average O3 

concentrations from hourly data, any calculated digits beyond the third decimal place would be truncated, preserving 

the number of digits in the reported data. In calculating 3-year averages of the fourth highest maximum 8-hour 

average concentrations, digits to the right of the third decimal place would also be truncated, preserving the number 

of digits in the reported data.")
138

without accounting for the use of averaging across three years, which adds a significant 

additional degree of under-protection, a 4th highest standard by definition allows three days per 

year during when ozone levels are unconstrained and are not considered in classifications of 

attainment. If ozone levels on these peak days are appreciably higher than on the 4th highest day, 

given EPA’s acknowledged concerns regarding single or multiple (defined by EPA as 2 or more) 

exposures to elevated ozone concentrations, EPA must account for the degree of underprotection in setting the level of the NAAQS. Stated another way, as discussed below, if EPA 

adopts a nominal level of 70 ppb but uses a fourth highest form, the result is a standard that is 

effectively a 77-78 ppb standard.

To determine the relationship between 1st, 2nd and 4th high ozone concentrations, we 

calculated the “design values” for five different three-year periods for each Core Based 

Statistical Area (CBSA) in the country as follows. For every ozone monitor in the United States, 

we pulled the 1st through 4th maximum 8-hour daily ozone levels for each year from 2008 to 

2014. For each CBSA and each three-year period (i.e., 2008-2010, 2009-2011, up to 2012-2014) 

we identified the “design value” for the CBSA under three different assumed forms of the 

standard: (1) the current 4th highest form (i.e., 3-year average of 4th highest 8-hour daily 

maximums using the monitor site in the CBSA for which this value is highest); (2) a 1st highest

form (i.e., 3-year average of 1st highest 8-hour daily maximums for the monitor site in the CBSA 

for which this value is highest; and (3) a 2nd highest form (i.e., 3-year average of 2nd highest daily 

8-hour maximums for the monitor site in the CBSA for which this value is highest). This 

provided three different design values for each three-year period from 2008-2010 to 2012-2014–

one based on the first highest, one based on the second highest, and one based on the fourth 

highest. For each of these three-year periods, we then examined both the ratio of the 1st , 2nd and 

4

th highest design value forms for each CBSA and also the absolute ppb difference between the 

1

st , 2nd and 4th highest design value forms for each CBSA. The tables below show the averages 

and standard deviations for the ratio and for the difference (see Exhibit 8).

Figure 12
139

Table 10

2010 Average Diff from 4th

Standard 

Deviation

4th highest CBSA design value 69.7672

1st highest CBSA design value 77.3780 7.6108 3.4602

2nd highest CBSA design value 73.6117 3.8445 2.0162

Average

Standard 

Deviation

Ratio of 1st to 4th highest CBSA design 

value 1.1083 0.0467

Ratio of 2nd to 4th highest CBSA design 

value 1.0548 0.0279

Table 11

2011 Average Diff from 4th

Standard 

Deviation

4th highest CBSA design value 69.7518

1st highest CBSA design value 77.3016 7.5498 3.4341

2nd highest CBSA design value 73.5679 3.8161 1.9936

Average

Standard 

Deviation

Ratio of 1st to 4th highest CBSA design 

value 1.1081 0.0465
140

Ratio of 2nd to 4th highest CBSA design 

value 1.0546 0.0278

Table 12

2012 Average Diff from 4th

Standard 

Deviation

4th highest CBSA design value 71.4171

1st highest CBSA design value 79.5074 8.0903 3.4710

2nd highest CBSA design value 75.3799 3.9628 1.8935

Average

Standard 

Deviation

Ratio of 1st to 4th highest CBSA design 

value 1.1126 0.0448

Ratio of 2nd to 4th highest CBSA design 

value 1.0551 0.0242

Table 13

2013 Average Diff from 4th

Standard 

Deviation

4th highest CBSA design value 69.4930

1st highest CBSA design value 77.3419 7.8489 3.4064

2nd highest CBSA design value 73.2508 3.7578 1.7766

Average

Standard 

Deviation

Ratio of 1st to 4th highest CBSA design 

value 1.1121 0.0444

Ratio of 2nd to 4th highest CBSA design 

value 1.0539 0.0236

Table 14

2014 Average Diff from 4th

Standard 

Deviation

4th highest CBSA design value 67.6946

1st highest CBSA design value 74.9183 7.2237 3.0649

2nd highest CBSA design value 71.1688 3.4742 1.5290

Average

Standard 

Deviation

Ratio of 1st to 4th highest CBSA design 

value 1.1065 0.0428
141

Ratio of 2nd to 4th highest CBSA design 

value 1.0514 0.0221

The results are remarkably consistent across time.402 For all three-year periods reviewed, 

the 4th highest design value is 7.2 to 8.1 ppb lower on average across CBSAs than a 1st highest

“design value” and 3.5 to 4.0 ppb lower on average across CBSAs than a 2nd highest “design 

value.” 

The consequences for public health protection are massive. Retaining the current form of 

the NAAQS and setting the level at 70 ppb is equivalent to establishing a 1st max standard of 

between 77.2 and 78.1 ppb. That means, under a standard of 70 ppb using the current form, 

occurrences of and exposures to 8-hour concentrations in the range of 77.2 to 78.1 ppb would be 

anticipated annually in areas just meeting the NAAQS. And likewise, with a 4th highest standard 

of 65 ppb, occurrences of and exposures to 8-hour concentrations of 72.2 to 73.1 ppb (as well as 

multiple exposures between 70 and 77.2) would be anticipated annually in areas just meeting the 

NAAQS. Individual exposures to all of these concentrations for only 6.6 hours were found to 

produce both lung function decrements and symptoms, a fact that EPA does not dispute and a 

combination of effects that EPA acknowledges to be adverse. Consequently, given the proposed 

form of the standard, EPA cannot support a level in the range of 65 to 70 ppb. 

Moreover, the above results illustrate that there will be multiple occurrences of ozone 

levels corresponding to exposures of concern in areas meeting a NAAQS of 65 to 70 ppb. The 

average 2nd highest “design value” for CBSAs ranges from 3.5 to 4 ppb higher than the 4th

highest design values. Consequently, for areas just meeting a standard of 70 ppb, there would be 

anticipated to be multiple 8-hour occurrences of levels of 73.5 ppb or higher each year—

exposures to which EPA acknowledges to be adverse based on controlled human exposures 

studies using exposures for only 6.6 hours. 

For the urban areas included in EPA’s Health Risk and Exposure Assessment, the 

differences between 1st, 2nd and 4th highest design values were even greater. Table 15 identifies 

the difference between 1st and 4th highest 3-year average design values for the three-year periods 

2008-2010 through 2012-2014. Table 16 identifies the difference between 2nd and 4th highest 3-

year average design values for the same five three-year periods. As the tables illustrate, the 

average difference between 1st and 4th highest design value across the five periods is 12.5 ppb. 

And the average difference between 2nd and 4th highest design value across the five periods is 6.1 

ppb. These data show that in order to account for the form of the standard, in these areas, the 

level of the standard would need to be set 12.5 ppb lower to avoid individual exposures to the 

level of the NAAQS and 6.1 ppb lower to avoid multiple exposures to that level.

Table 15: Differences Between 1st and 4th Highest-Based Design Values for EPA HREA 

Study Areas, 2008 to 2014

Area 1

st

-4

th

Design 

1

st

– 4

th

Design 

1

st

– 4

th

Design 

1

st

– 4

th

Design 

1

st

– 4

th

Design 

Average 1st

– 4

th Design 

 

402 These results are also consistent with California’s testimony that 70 ppb not to be exceeded standard is equivalent 

to a 60 ppb standard. 
142

Value 

2008-2010

(ppb)

Value 

2009-2011 

(ppb)

Value 

2010-2012

(ppb)

Value 

2011-2013

(ppb)

Value 

2012-2014

(ppb)

Value for 

2008 to 

2014

Atlanta-Sandy Springs-Marietta, 

GA

13.0 12.0 16.0 16.7 16.7 15.1

Baltimore-Towson, MD 18.0 18.7 16.7 14.7 19.3 17.5

Boston-Cambridge-Quincy, MANH8.7 10.0 13.0 12.0 10.0 10.7

Chicago-Naperville-Joliet, IL-INWI10.3 12.7 11.0 10.3 6.7 10.2

Cleveland-Elyria-Mentor, OH 10.0 11.3 12.3 14.3 12.7 12.1

Dallas-Ft. Worth-Arlington, TX 10.7 7.0 9.3 n/a n/a 9.0

Denver-Aurora, CO 7.3 12.3 14.0 12.0 6.7 10.5

Detroit-Warren-Livonia, MI 13.0 13.0 13.7 15.3 17.3 14.5

Houston-Sugar Land-Baytown, 

TX

15.7 15.0 15.3 18.0 19.0 16.6

Los Angeles-Long Beach-Santa 

Ana, CA

16.0 18.7 n/a n/a n/a 17.3

New York-Northern New JerseyLong Island, NY-NJ-PA8.7 12.7 14.7 16.0 14.3 13.3

Philadelphia-CamdenWilmington, PA-NJ-DE-MD11.0 8.7 9.3 7.0 9.7 9.1

Sacramento-Arden ArcadeRoseville, CA13.7 9.3 9.3 6.7 6.3 9.1

St. Louis, MO-IL 10.0 9.3 9.7 13.7 10.0 10.5

Washington-ArlingtonAlexandria, DC-VA-MD-WV13.7 10.3 13.7 10.3 9.0 11.4

Table 16: Differences Between 2nd and 4th Highest-Based Design Values for EPA HREA 

Study Areas, 2008 to 2014

Area 2

nd

-4

th

Design 

Value 

2008-2010

(ppb)

2

nd

– 4

th

Design 

Value 

2009-2011 

(ppb)

2

nd

– 4

th

Design 

Value 

2010-2012

(ppb)

2

nd

– 4

th

Design 

Value 

2011-2013

(ppb)

2

nd

– 4

th

Design 

Value 

2012-2014

(ppb)

Average 2nd

– 4

th Design 

Value for 

2008 to 

2014

Atlanta-Sandy Springs-Marietta, 

GA

9.7 9.3 5.3 7.0 5.7 7.4

Baltimore-Towson, MD 8.3 7.3 7.7 8.0 8.7 8.0

Boston-Cambridge-Quincy, MANH5.7 6.7 4.7 3.7 3.7 4.9

Chicago-Naperville-Joliet, IL-INWI6.0 7.3 5.3 4.0 3.0 5.1

Cleveland-Elyria-Mentor, OH 8.0 8.7 5.3 5.0 3.7 6.1

Dallas-Ft. Worth-Arlington, TX 5.0 5.0 7.0 n/a n/a 5.7

Denver-Aurora, CO 3.7 4.0 5.7 5.7 3.7 4.5

Detroit-Warren-Livonia, MI 5.3 4.7 5.3 6.3 5.3 5.4

Houston-Sugar Land-Baytown, 8.0 11.7 9.0 10.7 6.7 9.2
143

TX

Los Angeles-Long Beach-Santa 

Ana, CA

4.3 7.0 n/a n/a n/a 5.7

New York-Northern New JerseyLong Island, NY-NJ-PA5.0 8.3 10.3 10.0 4.7 7.7

Philadelphia-CamdenWilmington, PA-NJ-DE-MD6.3 4.7 7.7 3.7 4.7 5.4

Sacramento-Arden ArcadeRoseville, CA6.7 5.7 5.3 4.7 4.3 5.3

St. Louis, MO-IL 5.0 6.3 6.0 6.7 5.3 5.9

Washington-ArlingtonAlexandria, DC-VA-MD-WV5.3 5.0 7.7 3.3 2.3 4.7

c. Under EPA’s Proposed Form of the Standard, a Level of 65 to 

70 ppb Would Impermissibly Allow, in a Single Ozone Season, 

Numerous Exposures to Levels Far in Excess of Those 

Acknowledged to be of Concern without Triggering a 

Nonattainment Designation

The statistical analysis in the previous section is made concrete by considering monitored 

ozone data from CBSAs presently attaining standards of 70 and 65 ppb. Table 17 provides 

CBSAs with design values between 66 and 70 ppb —CBSAs that would be judged in attainment 

with a 70 standard--routinely record numerous days with maximum 8-hour concentrations of 70 

ppb or higher in a single year, and almost uniformly record multiple levels of 70 ppb or higher in 

a single calendar year.

403

 The Columbia, South Carolina area, for example, recorded up to 20 

days with 8-hour maximum concentrations of 70 ppb or higher in one year, yet still achieved a 3-

year design value of 69 ppb. Vineland-Millville-Bridgeton, New Jersey recorded 19 days in a 

single ozone season with 8 hour concentrations of 70 ppb or above while attaining a 3-year 

design value of 70 ppb. Cadillac, Michigan recorded 17 days in a single ozone season with 8 

hour levels of 70 ppb or higher but met a standard of 70 ppb. 

Indeed, across the nation there are untold numbers of areas that would be judged to be in 

compliance with a 70 ppb standard using the form that EPA is proposing—and that therefore 

would never have to clean its air or reduce pollution--but that would nonetheless regularly 

subject residents to 8 hour concentrations above 70 ppb standard: Pensacola, Florida recorded 

16 days of 70 ppb or above, Jefferson City, Missouri, 15 days, Athens, Georgia, Brigham City 

Utah, Clarksville, Kentucky, Columbia, Missouri, and Lafayette, Indiana all recorded 14 days, 

Clinton, Iowa and Omaha-Council Bluffs, Nebraska, 13 days, Madison, Wisconsin, HuntingtonAshland, West Virginia-Kentucky-Ohio and Huntsville, Alabama 12 days—yet all of these 

CBSAs had maximum design values of 70 ppb or lower. 

Nor are repeated occurrences in areas currently meeting a standard of 70 ppb limited to 

concentrations near 70 ppb. Millville, New Jersey registered 12 days with maximum 8-hour 

concentrations of 75 ppb or higher in a single ozone season while meeting a standard of 70 ppb. 

 

403 See Exhibit 10. 
144

Columbia, South Carolina recorded 10 days with maximum 8-hour concentrations of 75 ppb or 

higher in the same ozone season while meeting a 3-year average of 69 ppb. As a result, 

Columbia, South Carolina would be judged to be in attainment with a 70 ppb, would be allowed 

to maintain that level of ozone air pollution forever, and would not have to take any steps to 

reduce levels of ozone--despite the fact that residents would be repeatedly exposed to 8 hour 

ozone levels above 70 ppb which EPA has judged to be unsafe. Many areas recorded at least six 

days in a single ozone season with levels of 75 ppb or higher for 8 hours while still attaining at a 

level of 70 ppb including Akron, Ohio, Cadillac, Michigan, Clinton, Iowa, Columbia, Missouri, 

Fayetteville, North Carolina, Huntington-Ashland, WV-KY-OH, Huntsville, Alabama, OmahaCouncil Bluffs, Nebraska, Pensacola, Florida. 

Of even greater concern, many areas recorded multiple days with maximum 8-hour 

concentrations of 80 ppb or higher in a single season (Akron, OH; Anderson, SC; Athens, GA; 

Cadillac, MI; Clarksville, KY; Columbia, MO; Durham, NC; Elizabethtown, KY; Fayetteville, 

NC; Florence, SC; Gulfport-Biloxi, MS; Huntington-Ashland, WV-KY-OH; Huntsville, AL; 

Jackson, MS; Johnstown, PA; Lakeland, FL; Madison, WI; Muncie, IN; Parkersburg-MariettaVienna, WV-OH; Pensacola, FL; Poughkeepsie, NY; Quincy, IL-MO; Watertown-Ft. Drum, 

NY), yet attained a standard of 70 ppb. Columbia, South Carolina had 4 days in a single ozone 

season with 8 hour concentrations of 80 ppb or higher yet its design value was only 69 ppb. And 

Millville, NJ recorded 7 days in a single season with 8-hour ozone levels of 80 ppb or higher and 

attained a standard of 70 ppb. 

Indeed, some areas meeting a standard of 70 ppb even recorded levels of 85 ppb or 

higher.404 This was true in at least 38 CBSAs with design values between 66 and 70 ppb, 

including Millville, NJ, which recorded 3 days with 8 hour concentrations of 85 ppb or higher 

while attaining a standard of 70 ppb. Elkhart, Indiana recorded an 8-hour ozone concentration of 

111 ppb in 2012 yet attained a design value below 70 ppb for 2011 to 2013. 

 

404 See Exhibit 9. 
145

Table 17: 2011-2013 Ozone Monitor Data for CBSAs with Design Value 0.066 to 0.070 ppm (Monitors with Design Value 0.066 

to 0.070 ppm)

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Akron OH Portage Rockwell 391331001 0.067 11(8) 4(3) 1(1) 1(1)

Akron OH Summit Patterson Park 391530020 0.068 14(9) 7(6) 3(2) 2(1)

AlbanySchenectadyTroy

NY Albany Loudonville 360010012 0.067 9(8) 3(2) 2(1) 0(0)

Anderson IN Madison n/a 180950010 0.069 15(11) 3(3) 1(1) 1(1)

Anderson SC Anderson n/a 450070005 0.068 14(9) 7(4) 3(2) 2(1)

Asheville NC Haywood Purchase Knob 370870036 0.067 6(4) 3(2) 0(0) 0(0)

Athens GA Clarke Fire Station #7 130590002 0.068 18(14) 8(5) 2(2) 1(1)

AugustaRichmond GA Richmond Bungalow Rd. 132450091 0.069 14(8) 5(3) 1(1) 0(0)

AugustaRichmond GA Columbia Riverside Park 130730001 0.068 13(9) 6(3) 2(2) 1(1)

Baraboo WI Sauk Devils Lake SP 551110007 0.067 10(10) 2(2) 0(0) 0(0)

Berlin NH Coos Mt. Washington 330074001 0.069 12(6) 2(2) 0(0) 0(0)

Boise CityNampa ID Ada n/a 160010017 0.068 10(5) 3(2) 1(1) 0(0)

Brigham City UT Box Elder Brigham City 490030003 0.069 19(14) 3(2) 1(1) 0(0)

Cadillac MI Missaukee n/a 261130001 0.070 21(17) 9(8) 2(2) 0(0)

Chambersburg PA Franklin Methodist Hill 420550001 0.068 8(6) 2(1) 0(0) 0(0)

Clarksville KY Christian Hopkinsville 210470006 0.069 20(14) 5(5) 0(0) 0(0)

Clarksville KY Trigg Dover Rd. 212219991 0.070 14(12) 5(4) 3(3) 1(1)

Clinton IA Clinton Rainbow Park 190450021 0.068 15(13) 7(7) 0(0) 0(0)

Columbia MO Boone Finger Lakes 290190011 0.069 17(14) 7(7) 2(2) 1(1)
146

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Columbia SC Richland Sandhill Exp. Stn. 450791001 0.069 23(20) 11(10) 4(4) 1(1)

Corpus Christi TX Nueces Corp. Christi West 483550025 0.070 9(6) 5(4) 0(0) 0(0)

Corpus Christi TX Nueces CC Toluso 483550026 0.069 9(7) 4(3) 3(2) 1(1)

Dalton GA Murray Ft. Mtn. 132130003 0.068 12(8) 2(2) 0(0) 0(0)

DaphneFairhope-Foley AL Baldwin Fairhope 010030010 0.067 12(10) 2(2) 0(0) 0(0)

Decatur AL Morgan Decatur 11030011 0.068 12(7) 4(3) 0(0) 0(0)

Deming NM Luna Airport Rd. 350290003 0.067 6(5) 1(1) 0(0) 0(0)

Durham NC Person Bushy Fork 371450003 0.069 8(6) 5(5) 2(2) 0(0)

Durham NC Durham Durham Armory 370630015 0.068 11(7) 4(3) 1(1) 1(1)

Effingham IL Effingham Central Jr. High 170491001 0.067 12(11) 2(2) 1(1) 1(1)

Elizabethtown KY Hardin n/a 210930006 0.070 11(8) 3(3) 2(2) 1(1)

ElkhartGoshen IN Elkhart Bristol 180390007 0.067 14(9) 7(4) 2(1) 1(1)

Fayetteville NC Cumberland Golfview 370511003 0.069 14(10) 7(6) 4(3) 0(0)

Fayetteville NC Cumberland n/a 370510008 0.067 11(8) 3(2) 1(1) 0(0)

Fernley NV Lyon Fernley Intermed. 

School 320190006 0.069 10(6) 3(2) 1(1) 0(0)

Florence SC Darlington Pee Dee Exp. Stn. 450310003 0.066 11(7) 3(2) 2(2) 0(0)

Fort Payne AL DeKalb Sand Mtn. 010499991 0.066 6(5) 1(1) 0(0) 0(0)

Fort Wayne IN Allen Amstutz Rd. 180030002 0.069 12(8) 4(3) 1(1) 1(1)

Fort Wayne IN Allen N. Beacon 180030004 0.069 15(8) 5(3) 1(1) 1(1)

Grand Junction CO Mesa Rapid Creek Rd. 080770020 0.067 4(4) 2(2) 0(0) 0(0)

Greenville NC Pitt Pitt Ag. Ctr. 371470006 0.069 16(10) 5(3) 2(1) 1(1)

GreenvilleMauldinEasley

SC Greenville Hillcrest Middle 

School 450450016 0.067 7(4) 2(1) 1(1) 0(0)

GreenvilleMauldinSC Pickens Clemson CMS 450770002 0.067 11(10) 4(4) 1(1) 0(0)
147

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Easley

GulfportBiloxi MS Harrison Gulfport Youth 

Court 280470008 0.069 18(11) 4(2) 2(2) 0(0)

GulfportBiloxi MS Hancock Waveland 280450003 0.066 5(3) 1(1) 0(0) 0(0)

Harrison AR Newton 051010002 0.067 5(3) 2(2) 1(1) 0(0)

Hobbs NM Lew Hobbs-Jefferson 350250008 0.066 7(5) 0(0) 0(0) 0(0)

HuntingtonAshlandWV-KYOH Boyd Ashland Primary 

(FIVCO) 210190017 0.069 12(7) 6(3) 1(1) 0(0)

HuntingtonAshlandWV-KYOH Greenup Worthington 210890007 0.069 17(12) 8(6) 3(2) 2(1)

HuntingtonAshlandWV-KYOH Cabell

Henderson 

Center/Marshall 

University

540110006 0.069 17(10) 8(5) 3(2) 1(1)

HuntingtonAshlandWV-KYOH Lawrence ODOT (Ironton) 390870012 0.068 10(8) 5(4) 1(1) 1(1)

Huntsville AL Madison Huntsville Old 

Airport 010890014 0.070 17(12) 8(6) 2(2) 0(0)

Jackson MS Hinds Jackson FS19 280490010 0.066 6(4) 4(3) 2(2) 1(1)

Jefferson City MO Callaway New Bloomfield 290270002 0.068 17(15) 4(4) 1(1) 0(0)

Johnstown PA Cambria 420210011 0.070 15(9) 5(2) 2(2) 2(2)

Kinston NC Lenoir Lenoir Co. Comm. 

Coll. 371070004 0.067 6(3) 1(1) 1(1) 0(0)

Lafayette IN Carroll Flora-Flora Airport 180150002 0.069 15(14) 5(4) 1(1) 1(1)

Lafayette LA Lafayette Lafayette / USGS 220550007 0.069 13(6) 5(3) 1(1) 0(0)

Lake Charles LA Calcasieu Vinton 220190009 0.070 10(6) 5(3) 1(1) 0(0)

Lake Charles LA Calcasieu Carlyss 220190002 0.069 15(8) 2(1) 0(0) 0(0)

Lake Charles LA Calcasieu Westlake 220190008 0.067 6(3) 1(1) 1(1) 0(0)

Lakeland FL Polk 121056005 0.068 10(5) 3(2) 1(1) 1(1)
148

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Lakeland FL Polk Baptist Childrens' 

Home 121056006 0.068 10(5) 5(3) 4(3) 2(1)

Logan UT-ID Cache Logan #4 490050004 0.067 7(6) 1(1) 0(0) 0(0)

Madison WI Columbia Columbus 550210015 0.069 15(12) 2(2) 1(1) 1(1)

Madison WI Dane Madison East 550250041 0.069 11(10) 3(3) 2(2) 2(2)

ManchesterNashua NH Hillsborough Gibson Road 330111011 0.067 4(2) 3(2) 2(1) 2(1)

ManchesterNashua NH Hillsborough Miller State Park 330115001 0.067 10(6) 3(2) 0(0) 0(0)

MinneapolisSt. PaulBloomington

MN Anoka Anoka Airport 270031002 0.067 7(4) 4(2) 2(1) 1(1)

Minneapolis MN Anoka Cedar Creek 270031001 0.067 7(4) 2(2) 1(1) 1(1)

Mobile AL Mobile Chickasaw 010970003 0.066 7(4) 2(1) 0(0) 0(0)

Morgantown WV Monongalia 540610003 0.068 12(9) 4(2) 1(1) 1(1)

Muncie IN Delaware Albany- Albany 

Elem. Sch. 180350010 0.068 15(11) 4(4) 2(2) 0(0)

OmahaCouncil Bluffs IA Harrison Pisgah 190851101 0.069 15(13) 6(6) 0(0) 0(0)

OmahaCouncil Bluffs IA Harrison Woolworth 190850007 0.068 11(10) 4(4) 1(1) 0(0)

OmahaCouncil Bluffs NE Douglas n/a 310550019 0.067 8(4) 0(0) 0(0) 0(0)

Panama CityLynn Haven FL Bay St. Andrews State 

Park 120050006 0.066 7(5) 0(0) 0(0) 0(0)

ParkersburgMariettaVienna

WV-OH Washington Marietta Twp. 391670004 0.069 15(9) 5(4) 2(1) 1(1)

Parkersburg- WV-OH Wood Neale Elementary 541071002 0.068 14(10) 6(5) 3(2) 0(0)
149

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

MariettaViennaSchool

Pascagoula MS Jackson Pascagoula 280590006 0.070 23(11) 3(2) 0(0) 0(0)

PensacolaFerry PassBrent

FL Escambia n/a 120330018 0.070 21(16) 3(2) 0(0) 0(0)

PensacolaFerry PassBrent

FL Santa Rosa n/a 121130015 0.069 14(12) 6(6) 2(2) 0(0)

PensacolaFerry PassBrent

FL Escambia Ellyson Industrial 

Park 120330004 0.067 6(5) 1(1) 0(0) 0(0)

PoughkeepsieNewburghMiddletown

NY Dutchess Millbrook 360270007 0.070 10(5) 7(4) 2(2) 1(1)

Prescott AZ Yavapai Prescott College 

AQD 040258033 0.069 15(9) 1(1) 0(0) 0(0)

Price UT Carbon n/a 490071003 0.069 15(11) 4(3) 0(0) 0(0)

Quincy IL-MO Adams John Wood Comm. 

Coll. 170010007 0.068 8(6) 4(4) 2(2) 1(1)

Redding CA Shasta Lassen Volcanic 

Park 60893003 0.068 7(4) 3(3) 1(1) 0(0)

Redding CA Shasta Shasta Lake 60890009 0.067 7(5) 1(1) 0(0) 0(0)

Reno-Sparks NV Washoe Sparks 320311005 0.068 7(5) 3(2) 1(1) 0(0)

Reno-Sparks NV Washoe South Reno 320310020 0.068 7(5) 1(1) 0(0) 0(0)

Reno-Sparks NV Washoe Lemmon Valley 320312009 0.067 9(6) 3(2) 0(0) 0(0)

Reno-Sparks NV Washoe Reno 3 320310016 0.067 9(6) 1(1) 0(0) 0(0)

Reno-Sparks NV Washoe Toll 320310025 0.066 3(1) 0(0) 0(0) 0(0)

Riverton WY Fremont n/a 560130232 0.066 4(2) 0(0) 0(0) 0(0)
150

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Rock Springs WY Sweetwater Moxa 560370300 0.066 3(2) 0(0) 0(0) 0(0)

Rockford IL Winnebago Maple Elem. Schl. 172012001 0.068 9(7) 3(2) 0(0) 0(0)

Rockland ME Knox Marshall Point 

Lighthouse 230130004 0.068 8(5) 5(4) 1(1) 0(0)

Rocky Mount NC Edgecombe Leggett 370650099 0.069 13(8) 3(2) 1(1) 1(1)

Santa Fe NM Santa Fe n/a 350490021 0.066 5(3) 0(0) 0(0) 0(0)

ScrantonWilkes Barre PA Luzerne n/a 420690101 0.070 6(4) 3(3) 1(1) 0(0)

ScrantonWilkes Barre PA Luzerne n/a 420692006 0.069 6(4) 3(3) 0(0) 0(0)

Show Low AZ Navajo

Petrified Forest 

National Park, 

South Entrance

040170119 0.070 12(8) 2(2) 0(0) 0(0)

Sioux Falls SD Minnehaha SD School for the 

Deaf 460990008 0.068 11(10) 1(1) 0(0) 0(0)

Somerset KY Pulaski Somerset 211990003 0.067 7(5) 4(4) 1(1) 0(0)

Syracuse NY Onondaga East Syracuse 360671015 0.069 10(8) 3(2) 1(1) 0(0)

Syracuse NY Oswego Fulton 360750003 0.067 6(4) 3(2) 0(0) 0(0)

Terre Haute IN Vigo

Terre Haute CAAP/ 

McLean High 

School

181670018 0.067 14(13) 5(4) 1(1) 0(0)

VallejoFairfield CA Solano Ground in shelter 060953003 0.067 10(5) 1(1) 1(1) 0(0)

Victoria TX Victoria Victoria 484690003 0.067 7(6) 2(2) 1(1) 0(0)

VinelandMillvilleBridgeton

NJ Cumberland Millville 340110007 0.070 21(19) 14(12) 7(7) 3(3)

WatertownFort Drum NY Jefferson Perch River 360450002 0.070 13(10) 7(5) 2(2) 0(0)
151

CBSA State County Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr)

Total 

days 

75+ ppb 

(max/yr)

Total 

days 

80+ ppb 

(max/yr)

Total 

days 

85+ ppb 

(max/yr)

Williamsport PA Lycoming Montoursville 420810100 0.066 8(7) 0(0) 0(0) 0(0)

Worcester MA Worcester Uxbridge 250270024 0.068 10(4) 3(2) 1(1) 1(1)

Worcester MA Worcester Worcester Airport 250270015 0.067 9(4) 3(2) 2(1) 2(1)
152

Setting the standard at 65 ppb does not eliminate occurrences of 70 ppb, or even multiple 

occurrences of 70 ppb in a single ozone season. Numerous CBSAs with design values of 65 ppb 

and below record multiple 8-hour concentrations of 70 ppb or higher in a single ozone season. 

As illustrated in Table 18 below, Sault Ste. Marie, Michigan, recorded 9 days with 8-hour 

average ozone concentrations of 70 ppb or higher in a single ozone season yet had a 2011-2013 

design value of only 0.064 ppm. Likewise, Florence-Muscle Shoals, Alabama and Gillette, 

Wyoming recorded 8 days in a single season with 8-hour concentrations of 70 ppb or above yet 

still attained a standard of 65 ppb. Sault Ste. Marie, Florence-Muscle Shoals, and Seattle, 

Washington, all recorded multiple days with 8-hour concentrations of 80 ppb or above in a single 

ozone season while attaining a standard of 65 ppb or lower for 2011-2013. 

Not only would a standard of 65 fail to eliminate multiple occurrences of 70 and even 80 

ppb during a single year, a standard of 65 ppb would do even less to eliminate instances of 

multiple exposures to 8-hour ozone concentrations of 60 ppb, contrary to EPA’s suggestion.405 

As Table 18 identifies, CBSAs with 2011-2013 design values that would be meeting a standard 

of 65 ppb (including all CBSAs with design values of exactly 65 ppb) routinely record dozens of 

days in a season with peak 8-hour concentrations of 60 ppb or above. Gillette, Wyoming had as 

many as 51 days in a single ozone season on which ozone concentrations were 60 ppb or above; 

yet Gillette still attained a standard of 65 ppb. Gillette is by no means alone. Evanston, Illinois 

had 46 days in a single season of 8-hour ozone levels of 60 ppb or higher; Cedar Rapids, Iowa 

had 40 days; Roanoke, Virginia had 34 days; Winchester VA-WV had 32. 

 

405 See Exhibit 11.
153

Table 18: 2011-2013 Ozone Monitor Data for CBSAs with Design Values 0.062 ppm - 0.065 ppm (Monitors with Design Values 0.062 ppm -

0.065 ppm)

CBSA State County Monitor Site Name Monitor Site ID

Monitor 

Design 

Value 

(ppm)

Total

days 60+ 

ppb 

(max/yr)

Total days 

65+ ppb 

(max/yr)

Total 

days 

70+ 

ppb 

(max 

/yr)

T

da

(m

Cedar Rapids IA Linn Kirkwood 191130028 0.065 57(40) 24(19) 6(6) 1(

Charlottesville VA Albemarle Albemarle High School 391530020 0.065 45(23) 12(6) 3(2) 1(

Columbus GAAL Russell Ladonia, Phenix City 011130002 0.065 54(27) 21(10) 3(2) 1(

Des Moines-West Des Moines IA Warren

Gravel Road in Lake Aquabi State 

Park 191810022 0.064 43(32) 17(16) 7(7)

Evanston WY Uinta Murphy Ridge 560410101 0.065 66(46) 16(8) 3(3) 1(

Florence-Muscle Shoals AL Colbert Muscle Shoals 10331002 0.064 41(23) 15(13) 8(8) 2(

Gillette WY Campbell Thunder Basin 560050123 0.064 68(51) 30(27) 8(8)

Hickory-Lenoir-Morganton NC Alexander Waggin` Trail 370030004 0.065 47(22) 15(6) 6(3)

Huntington IN Huntington Roanoke- Roanoke Elem. School 180690002 0.065 39(19) 15(9) 6(3) 2(

Jackson WYID Teton Yellowstone National Park, Water 

Tank 560391011 0.065 66(27) 10(6) 3(2)

Marshall MN Lyon Marshall Airport 270834210 0.065 36(15) 13(6) 6(3)

Montgomery AL Montgomery MOMS, ADEM 11011002 0.065 54(31) 24(17) 5(5)

Roanoke VA Roanoke East Vinton Elementary School 511611004 0.064 64(34) 23(12) 6(4) 1(

Rochester NY Wayne Williamson 361173001 0.065 42(25) 25(16) 7(7)

Santa Barbara-Santa Maria-Goleta CA Santa Barbara Paradise Road 60831014 0.065 43(16) 16(7) 6(3) 2(

Santa Barbara-Santa Maria-Goleta CA Santa Barbara Los Flores Canyon #1 060831025 0.063 20(11) 9(5) 5(3) 2(

Sault Ste. Marie MI Chippewa North of Easterday Avenue 260330901 0.064 24(17) 12(10) 9(9) 8(

Seattle-Tacoma-Bellevue WA Warren Enumclaw-Mud Mtn 530330023 0.062 15(10) 10(7) 6(5) 2(
154

Sebastian-Vero Beach FL Indian River Indian River Lagoon 120619991 0.065 32(11) 11(4) 1(1)

Seymour IN Jackson

Brownstown- 225 W & 200 N. 

Water facility 180710001 0.065 30(12) 10(4) 3(1) 1(

Somerset PA Somerset Laurel Hill 421119991 0.065 41(19) 20(10) 4(2) 2(

Summerville GA Chattooga Summerville-DNR Fish Hatchery 130550001 0.065 41(20) 16(9) 5(3) 1(

Tallahassee FL Leon Tallahassee Community College 120730012 0.065 39(19) 17(9) 1(1)

Wausau WI Marathon Lake Dubay 550730012 0.065 36(19) 13(8) 4(3)

Winchester VAWV Frederick Rest 510690010 0.065 51(32) 23(14) 8(6) 1(
155

EPA’s proposal tries to avoid the empirical data that show repeated (and under the 

proposed form, permissible) 8-hour events of unsafe ozone levels over and above whatever level 

of ozone that EPA ultimately decides the health studies demonstrate will cause harm. Rather 

than determining what level of ozone is safe and creating a numerical standard and form that 

requires the country to achieve that level everywhere, all the time, by eliminating ozone events 

that exceed that level, EPA introduces the concept of “exposures” and swaps out “events” (of 

“occurrences”) for “exposures.” That is, EPA is proposing a standard that ensures that there are 

repeated, “permissible” 8 hour events of unsafe ozone levels—that is, ozone that is above 

whatever level EPA ultimately decides is the safe level based on the science--but EPA asserts 

this is acceptable because regardless if the air is in fact unsafe to breathe, no one will really be 

outside to be “exposed” to the events. 

To this end, EPA explains that “the Administrator places the most weight on estimates of 

two or more exposures of concern (i.e., as a surrogate for the occurrence of repeated exposures), 

though she also considers estimates of one or more, particularly for the 70 and 80 ppb 

benchmarks.”406 In proposing a range of 65 to 70 ppb, EPA notes that selecting 65 would place 

greater weight on, among other things, “[e]liminating almost all exposures of concern (even 

single occurrences) at or above 70 and 80 ppb; even in worst-case years and locations,” and 

“almost eliminating the occurrence of two or more exposures of concern at or above 60 ppb.”407 

Whereas, EPA notes that selecting a level at or near 70 ppb gives greater weight, among other 

things, to “[a]lmost eliminating the occurrence of two or more exposures of concern at or above 

70 and 80 ppb, even in the worst-case year and location.”408 

As the above tables illustrate, a standard of 65 ppb, for example, would neither eliminate 

almost all events of ozone levels at or above 70 and 80 ppb, nor eliminate occurrence of two or 

more events at or above 60 ppb. Indeed, events of 70 and 80 ppb would regularly occur at a 

nominal standard of 65 using EPA’s proposed form, and areas meeting a level of 65 ppb also 

routinely record numerous concentrations of levels above 60 ppb in a single year. 

The only way for EPA to reconcile the empirical data of the number of 8 hour events 

with unsafe levels of ozone—relative to whatever ultimate numerical standard EPA decides is 

safe—is to substitute regulation of the amount of air pollution in the air and the number of events 

of unsafe air with the number of times EPA estimates people will be exposed to that unsafe air. 

Even if this was not entirely unlawful, as discussed above, the bases for EPA’s exposure 

estimates is technically flawed and based on speculation associated with a small set of diaries as 

to whether people were or were not engaging in protective behavior when they made entries, and

whether the individuals’ experiences were reflective of sensitive populations such as outdoor 

workers or children at outdoor summer camps. 

Likewise, EPA’s assertion that a level of 70 ppb would “[a]most eliminat[e] the 

occurrence of two or more exposures of concern at or above 70 and 80 ppb, even in the worstcase year and location,” is wholly inconsistent with the empirical data of the number of events, 

 

406 Proposed Rule at 75,290. 

407 Id. at 75,309. 

408 Id. 
156

and is based on risk and exposure assessments that are flawed, CBSAs attaining a level of 70 ppb 

routinely record numerous events of 8-hour concentrations of 70 ppb or higher in a single year 

(indeed up to 20 such occurrences), and frequently record occurrences of concentrations of 80 or 

even 85 ppb. And EPA admits that its estimates of exposure could be off by wide margins—as 

much as 30% for various sensitive populations—and that it does not know to what extent, for 

example, averting behaviors were engaged in in the dairies it relied upon. Based on the form of 

the standard, EPA is simply incorrect to suggest that a standard of 70 ppb would “almost 

eliminate” events of concern at or above 70 and 80 ppb, and it is engaging in inadequately 

supported estimates in its exposure analysis. 

Nor can the extraordinary number of occurrences of concentrations of 70 ppb and above 

in areas meeting cannot be attributed to the fact that 70 ppb is below the current NAAQS. 

Replicating the analysis for areas just meeting the current NAAQS—i.e., those CBSAs with 

maximum 2011-2013 design values of 71 to 75 ppb robustly illustrates this point. Achieving the 

current standard fails to eliminate occurrences of multiple exposures to levels at and above the 

NAAQS, as EPA suggests would occur under a standard of 65 or 70 ppb. Nor does it eliminate, 

or even meaningfully limit, occurrences of multiple exposures to levels 5 ppb below the 

NAAQS, as EPA suggests would occur under a standard of 65 ppb. The table below starkly 

illustrates this fact. 

As is apparent across CBSAs, attaining the current 75 ppb standard fails to limit multiple 

exposures in a single ozone season to levels of 75 ppb and does not meaningfully constrain levels 

of 70 ppb. No CBSA had a 2011-2013 design value between 71 and 75 ppb and did not have 

multiple 8-hour daily maximum ozone levels of 75 or above in a single year. Indeed, most areas 

had numerous days with maximum 8-hour ozone levels of 75 or above. For example, 

Shreveport-Bossier City, LA had 17 in a single season with maximum 8-hour ozone 

concentrations of 75 ppb or higher and Dover, DE, Adrian, MI, and Las Cruces, NM had up to 

16 such days in a season. Table 19 identifies the 25 CBSAs that had at least 10 days in a single 

ozone season with maximum 8-hour ozone concentrations of 75 ppb or above that nevertheless 

attained the current 75 ppb ozone standard and therefore are not required to further clean up their 

emissions. And similar results follow from more recent 3 year design values such as 2012-2014.

Table 19: Maximum days during single ozone season with 8-hour ozone levels of 75 ppb or 

higher among CBSAs with a 2011-2013 design value between 71 and 75 ppb

Days in single ozone season with 8-

hour ozone level of 75 ppb or 

higher

CBSA

17 Shreveport-Bossier City, LA

16 Dover, DE

Adrian, MI

Las Cruces, NM

15 Flint, MI

Kalamazoo-Portage, MI

Traverse City, MI

14 Mount Vernon, IL

Lima, OH

Indiana, PA
157

13 Paducah, KY-IL

Ann Arbor, MI

Grand Rapids-Wyoming, MI

Salisbury, NC

12 Indianapolis-Carmel, IN

Erie, PA

Lancaster, PA

Knoxville, TN

Beaumont-Port Arthur, TX

11 Springfield, MO

Jamestown-Dunkirk-Fredonia, NY

10 Payson, AZ

Peoria, IL

Bowling Green, KY

Cambridge, MD

As Table 22 illustrates, attaining a standard of 75 ppb does not eliminate the occurrence of 

multiple exceedances in a single season of 8-hour ozone levels 5, 10 and even 15 or more ppb 

above the standard. Dover, DE and Ann Arbor, MI both have 10 days in a single season with 8-

hour ozone levels of 80 ppb or above yet have attained a standard of 75 ppb. Table 20 illustrates 

the 17 CBSAs attaining a standard of 75 ppb that nevertheless had at least six days in a single 

ozone season with 8-hour ozone levels of 80 ppb or above. Yet none of these areas are under 

any obligation to take further steps to reduce their pollution levels any further—and residents of 

these areas will therefore be repeatedly subjected to events with 8 hour ozone levels above 75 

ppb as the status quo going forward--despite the fact that EPA has determined that levels above 

75 ppb for more than 8 hours is harmful. 

Stated another way, EPA determined in 2008 that the health science indicates that 

exposures to ozone levels above 75 ppb for longer than 8 hours will result in adverse health 

impacts. EPA nonetheless created a 2008 NAAQS standard with a nominal numerical level of 

75 ppb but with a form—the same form EPA proposes to use again in this proceeding—that 

ensures numerous 8 hour ozone events far above that level with no further steps required by EPA 

to reduce that air pollution. And EPA is proposing to do the same thing again in this proceeding. 

Table 20: Maximum days during single ozone season with 8-hour ozone levels of 80 ppb or 

higher among CBSAs with a 2011-2013 design value between 71 and 75 ppb

Days in single ozone season with 8-

hour ozone level of 80 ppb or 

higher

CBSA

10 Dover, DE

Ann Arbor, MI

9 Flint, MI

Indiana, PA

8 Adrian, MI

7 Paducah, KY-IL

Shreveport-Bossier City, LA

Grand Rapids-Wyoming, MI
158

Traverse City, MI

Knoxville, TN

Beaumont-Port Arthur, TX

6 Mount Vernon, IL

Indianapolis-Carmel, IN

Baton Rouge, LA

Erie, PA

Lancaster, PA

Multiple single season events in areas meeting the current standard of 75 ppb are not 

limited to levels of 80 ppb and up. Eight CBSAs had four or more days in a single ozone season 

with maximum 8-hour ozone levels of 85 ppb or above: Dover, DE (7 days); Paducah, KY-IL 

and Adrian, MI (6 days); Shreveport-Bossier City, LA (5 days); Mount Vernon, IL, Ann Arbor, 

MI. Flint, MI, and Green Bay, WI (4 days). And 11 CBSA had multiple days in a single ozone 

season with maximum 8-hour ozone levels of 90 ppb or above, yet still attained the current 75 

ppb NAAQS during 2011 to 2013. These areas were Paducah, KY-IL, Morristown, TN, 

Beaumont-Port Arthur, TX, and Charleston, WV (3 days of 90 ppb or above in a single ozone 

season); and Dover, DE, Adrian, MI, Flint, MI, Kalamazoo-Portage, MI, Altoona, PA, 

Richmond, VA, and Green Bay, WI (2 days of 90 ppb or above in a single ozone season). 

CBSAs attaining a standard of 75 ppb even had days during the ozone season where maximum 

8-hour ozone concentrations were as high as 111409 and 112 ppb.410 These levels are 36 and 37 

ppb above the level of the NAAQS. 

Finally, although EPA contends that setting a NAAQS of 65 ppb will largely eliminate 

exposures of even 60 ppb, this is flatly contradicted by empirical data for areas meeting a 

standard of 75 ppb that show repeated events of 70 ppb and above. EPA must then rely on its 

flawed exposure analysis to try to reconcile the difference between how safe the air needs to be 

and how safe EPA’s proposed standard would actually make it. EPA is saying that meeting a 

standard of 65 ppb will largely eliminate exposures to levels 5 ppb lower. But for CBSAs with a 

design value between 71 and 75 ppb—i.e., those areas meeting a standard of 75 ppb—there can 

be dozens of days on which maximum 8-hour ozone concentrations are 70 ppb or higher. At 

least five CBSAs had more than 30 days in a single ozone season during which maximum 8-hour 

concentrations were 70 ppb or above, and an additional 26 CBSAs with design values between 

71 and 75 ppb had 20 or more days during a single season on which 8-hour ozone concentrations 

were 70 ppb or above. Table 21 below characterizes these areas. 

Table 21: Maximum days during single ozone season with 8-hour ozone levels of 70 ppb or 

higher among CBSAs with a 2011-2013 design value between 71 and 75 ppb

Days in single ozone season with 8-

hour ozone level of 70 ppb or 

higher

CBSA

36 Knoxville, TN

35 Las Cruces, NM

33 Payson, AZ

 

409 Salisbury, NC 8-hour daily maximum in 2012; Morristown, TN 8-hour daily maximum in 2012.

410 Beaumont-Port Arthur, TX 8-hour daily maximum in 2012.
159

Shreveport-Bossier City, LA

31 Adrian, MI

28 Chico, CA

Vicennes, IN

27 Mount Vernon, IL

26 Peducah, KY-IL

25 Indianapolis-Carmel, IN

Topeka, KS

Traverse City, MI

Lima, OH

McAlester, OK

Ogden-Clearfield, UT

23 Springfield, OH

22 Bloomington-Normal, IN

Bishop, CA

Baton Rouge, LA

21 Dover, DE

Ann Arbor, MI

Grand Rapids-Wyoming, MI

Kalamazoo-Portage, MI

Springfield, MO

Albuquerque, NM

Salisbury, NC

Tyler, TX

20 Lexington-Fayette, KY

Cambridge, MD

Beaumont-Port Arthur, TX

Waco, TX

Nor does the fact that the 75 ppb 2008 NAAQS is not fully attained diminish the import 

of these empirical data. Again, areas presently meeting the 75 ppb NAAQS are not required to 

further improve their air quality under the present standard. Moreover, it is worth noting that 

NAAQS are not attained overnight. Eighteen years out from the 1997 NAAQS, this standard is 

still not fully attained, even in areas that were supposed to attain the NAAQS much earlier based 

on the timelines set forth in the Clean Air Act. 
160

Table 22: 2011-2013 Ozone Monitor Data for CBSAs with Design Value 0.071 to 0.075 ppm (Monitors with Design Value 0.071 to 0.075 ppm)

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

AZ Coconino Flagstaff, AZ Grand Canyon National Park, The 

Abyss 040058001 0.072 26 (15) 7 (3) 1 0 0

AZ Gila Payson, AZ TONTO NM 040070010 0.075 43 (33) 17 (10) 3 (1) 0 0

AZ Cochise Sierra Vista-Douglas, AZ CHIRICAHUA NATIONAL MONUMENT 040038001 0.073 32 (15) 6 (4) 0 0 0

AZ Pima Tucson, AZ SAGUARO PARK 040190021 0.073 24 (13) 6 (4) 1 0 0

AZ Pima Tucson, AZ FAIRGROUNDS 040191020 0.071 14 (8) 2 (1) 0 0 0

AR Washington Fayetteville-SpringdaleRogers, AR-MO SPRINGDALE 051430005 0.072 25 (17) 9 (5) 4 (2) 0 0

CA Inyo Bishop, CA

DEATH VALLEY NATIONAL 

MONUMENT NEAR NEVARES 

SPRINGS ACCESS ROAD

060270101 0.072 35 (22) 8 (6) 0 0 0

CA Butte Chico, CA TEMPORARY STATION FOR SPECIAL 

STUDY OF O3 TRANSPORT 060070007 0.075 55 (28) 19 (9) 5 (2) 1 1

CA Tuolumne Phoenix Lake-Cedar 

Ridge, CA 251 S BARRETTA, SONORA, CA 95370 061090005 0.073 39 (19) 6 (4) 1 0 0

CA Tehama Red Bluff, CA Old Fire Lookout on top of Tucson 

Butte 061030004 0.074 42 (18) 13 (6) 3 (2) 0 0

CA Tehama Red Bluff, CA RED BLUFF-TEHAMA COUNTY 

SHERIFF'S OFFICE 061030005 0.072 18 (8) 6 (4) 1 1 0

CA Alameda San Francisco-OaklandFremont, CA Livermore – Rincon 060010007 0.071 17 (9) 8 (3) 3 (2) 1 1

CO El Paso Colorado Springs, CO U.S. AIR FORCE ACADEMY 080410013 0.074 26 (12) 4 (2) 2 (1) 0 0

CO El Paso Colorado Springs, CO MANITOU SPRINGS 080410016 0.074 27 (15) 5 (2) 1 0 0

CO La Plata Durango, CO 080671004 0.072 18 (15) 7 (7) 1 0 0
161

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

DE Kent Dover, DE PROPERTY OF KILLENS POND STATE 

PARK; BEHIND FARM BUILDINGS 100010002 0.074 30 (21) 19 (16) 12 (10) 9 (7) 2 (2)

FL Sarasota

Bradenton-SarasotaVenice, FL 121151005 0.071 14 (7) 6 (4) 1 0 0

FL Orange Orlando-Kissimmee, FL WINTER PARK 120952002 0.071 14 (8) 7 (5) 1 0 0

FL Hillsborough Tampa-St. PetersburgClearwater, FL 120570081 0.071 15 (10) 6 (4) 1 0 0

GA Bibb Macon, GA Macon SE 130210012 0.071 25 (17) 11 (8) 5 (3) 1 0

IL McLean Bloomington-Normal, IL ISU HARRIS PHYSICAL PLANT 171132003 0.072 26 (22) 9 (7) 3 (2) 0 0

IL Champaign Champaign-Urbana, IL BOOKER T. WASHINGTON ES 170190007 0.071 13 (7) 8 (4) 4 (3) 1 0

IL Macon Decatur, IL IEPA TRAILER 171150013 0.071 16 (11) 5 (4) 0 0 0

IL Hamilton Mount Vernon, IL TEN MILE CREEK DNR OFFICE 170650002 0.074 34 (27) 17 (14) 6 (6) 4 (4) 1

IL Peoria Peoria, IL PEORIA HEIGHTS HS 171431001 0.071 25 (22) 11 (10) 3 (2) 1 0

IL Sangamon Springfield, IL Illinois Building State Fairgrounds 171670014 0.072 21 (15) 11 (7) 3 (2) 1 0

IN Shelby Indianapolis-Carmel, IN TRITON Middle SCHOOL, NORTH OF 

FAIRLAND 181450001 0.075 28 (19) 16 (12) 7 (5) 2 (2) 0

IN Marion Indianapolis-Carmel, IN Indpls.- E. 16th St. 180970073 0.074 39 (25) 15 (10) 7 (6) 2 (2) 1

IN Boone Indianapolis-Carmel, IN Perry Worth ELEMENTRY SCHOOL, 

WEST OF WHITESTOWN 180110001 0.073 23 (17) 11 (9) 5 (4) 2 (1) 1

IN Marion Indianapolis-Carmel, IN Indpls- Washington Park/ in parking 

lot next to police station 180970078 0.072 24 (14) 10 (7) 3 (3) 1 0

IN Knox Vincennes, IN Vincennes 180839991 0.073 35 (28) 13 (9) 6 (3) 2 (2) 0

KS Shawnee Topeka, KS KNI 201770013 0.073 39 (25) 14 (9) 3 (3) 1 0

KY Edmonson Bowling Green, KY Mammoth Cave National Park, 

Houchin Meadow 210610501 0.071 22 (17) 10 (10) 4 (4) 1 1

KY Fayette Lexington-Fayette, KY LEXINGTON PRIMARY 210670012 0.071 26 (20) 13 (9) 3 (2) 1 0
162

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

KY Livingston Paducah, KY-IL SMITHLAND 211390003 0.074 31 (26) 15 (13) 7 (7) 5 (5) 2 (2)

KY McCracken Paducah, KY-IL JACKSON PURCHASE (PADUCAH 

PRIMARY) 211451024 0.074 32 (26) 19 (16) 10 (9) 7 (6) 3 (3)

LA East Baton 

Rouge Baton Rouge, LA LSU 220330003 0.075 35 (22) 11 (6) 7(4) 4 (2) 2 (1)

LA Iberville Baton Rouge, LA Carville 220470012 0.075 25 (16) 10 (7) 7 (6) 2 (2) 0

LA Pointe 

Coupee Baton Rouge, LA New Roads 220770001 0.074 26 (13) 14 (8) 3 (2) 2 (1) 0

LA East Baton 

Rouge Baton Rouge, LA Capitol 220330009 0.072 23 (14) 8 (6) 5 (4) 4 (3) 1

LA Livingston Baton Rouge, LA French Settlement 220630002 0.072 24 (15) 6 (4) 2 (1) 1 0

LA Ascension Baton Rouge, LA Dutchtown 220050004 0.071 20 (13) 8 (7) 4 (4) 3 (3) 0

LA Iberville Baton Rouge, LA Bayou Plaquemine 220470009 0.071 28 (14) 11 (7) 3 (3) 1 0

LA Lafourche Houma-Bayou CaneThibodaux, LA Thibodaux 220570004 0.071 15 (8) 8 (5) 2 (1) 0 0

LA St. John the 

Baptist

New Orleans-MetairieKenner, LA Garyville 220950002 0.072 26 (14) 13 (7) 1 1 0

LA St. Tammany New Orleans-MetairieKenner, LA Madisonville 221030002 0.072 23 (15) 11 (7) 3 (2) 1 0

LA Bossier Shreveport-Bossier City, 

LA Shreveport / Airport 220150008 0.074 40 (33) 19 (17) 8 (7) 5 (5) 0

LA Caddo Shreveport-Bossier City, 

LA Dixie 220170001 0.073 29 (23) 10 (7) 4 (4) 0 0

ME York Portland-South 

Portland-Biddeford, ME

KPW - Kennebunkport Parson'd Way 230312002 0.075 16 (7) 10 (4) 4 (2) 1 0

MD Dorchester Cambridge, MD Blackwater NWR 240199991 0.075 31 (20) 14 (10) 6 (4) 2 (1) 0

MD Washington Hagerstown- Hagerstown 240430009 0.071 22 (12) 7 (3) 3 (2) 1 0
163

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

Martinsburg, MD-WV

MA Barnstable Barnstable Town, MA TRURO NATIONAL SEASHORE 250010002 0.072 15 (8) 8 (6) 3 (3) 2 (2) 1

MA Norfolk Boston-CambridgeQuincy, MA-NH BLUE HILL OBSERVATORY 250213003 0.072 17 (8) 6 (3) 1 0 0

MA Essex Boston-CambridgeQuincy, MA-NH LYNN WATER TREATMENT PLANT 250092006 0.071 17 (7) 6 (2) 2 (1) 2 (1) 1

MA Hampden Springfield, MA WESTOVER AFB 250130008 0.073 20 (11) 7 (3) 3 (1) 0 0

MI Lenawee Adrian, MI 6792 RAISIN CENTER HWY, LENAWEE 

CO.RD.COMM.OWNER, TECUMSEH 260910007 0.075 45 (31) 22 (16) 10 (8) 7 (6) 2 (2)

MI Washtenaw Ann Arbor, MI TOWNER ST, SOUTH; 2 LANE 

RESIDENIAL – HOSPITAL 261610008 0.075 31 (21) 18 (13) 11 (10) 5 (4) 1

MI Genesee Flint, MI 260490021 0.074 26 (19) 17 (15) 10 

(9) 4 (4) 2 (2)

MI Genesee Flint, MI Otisville 260492001 0.074 26 (19) 14 (11) 6 (5) 4 (3) 1

MI Kent Grand Rapids-Wyoming, 

MI GR-Monroe 260810020 0.074 27 (19) 17 (12) 8 (7) 1 0

MI Kent Grand Rapids-Wyoming, 

MI

APPROXIMATELY 1/4 MILE SOUTH OF 

14 MILE RD 260810022 0.074 28 (21) 18 (13) 5 (3) 1 0

MI Kalamazoo Kalamazoo-Portage, MI KALAMAZOO FAIRGROUNDS 260770008 0.075 30 (21) 19 (15) 8 (7) 3 (3) 2 (2)

MI Ingham Lansing-East Lansing, MI 260650012 0.072 21 (16) 10 (9) 5 (5) 0 0

MI Clinton Lansing-East Lansing, MI ROSE LAKE, STOLL RD.(8562 E.) 260370001 0.071 19 (13) 11 (9) 3 (3) 3 (3) 1

MI Benzie Traverse City, MI 260190003 0.074 34 (25) 18 (15) 9 (7) 0 0

MS Bolivar Cleveland, MS Cleveland 280110001 0.071 16 (9) 7 (4) 0 0 0

MO Greene Springfield, MO Fellows Lake 290770042 0.072 31 (21) 13 (11) 4 (4) 0 0

MO Andrew St. Joseph, MO-KS Savannah 290030001 0.073 32 (19) 14 (7) 6 (5) 1 0

NJ Atlantic Atlantic City, NJ Brigantine 340010006 0.073 20 (11) 8 (4) 5 (3) 3 (2) 0
164

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

NM Bernalillo Albuquerque, NM Foothills 350011012 0.072 40 (21) 9 (5) 3 (2) 0 0

NM Bernalillo Albuquerque, NM WESTSIDE TAYLOR RANCH 350010027 0.071 25 (12) 4 (2) 0 0 0

NM Eddy Carlsbad-Artesia, NM

5ZR ON BLM LAND BORDERING 

RESIDENTIAL AREA OUTSIDE 

CARLSBAD CITY LIM

350151005 0.071 15 (8) 4 (2) 0 0 0

NM San Juan Farmington, NM 350450018 0.071 24 (12) 3 (3) 1 0 0

NM Dona Ana Las Cruces, NM

6ZN US-MEXICO BORDER CROSSING. 

BOTH SIDES UNINHABITED AS OF 

1996.

350130022 0.075 52 (35) 22 (16) 6 (4) 1 0

NM Dona Ana Las Cruces, NM

6ZM 2MI FROM MT CRISTO REY 

WHERE NM, TEX, AND MEXICO JOIN 

TOGETHER

350130021 0.072 22 (8) 7 (4) 2 (2) 0 0

NY Niagara Buffalo-Niagara Falls, NY MIDDLEPORT 360631006 0.073 22 (16) 9 (7) 5 (4) 2 (1) 1

NY Erie Buffalo-Niagara Falls, NY AMHERST 360290002 0.072 21 (14) 12 (8) 3 (3) 1 0

NY Chautauqua Jamestown-DunkirkFredonia, NY DUNKIRK 360130006 0.072 19 (14) 15 (11) 5 (4) 3 (2) 1

NC Guilford Greensboro-High Point, 

NC Mendenhall School 370810013 0.072 26 (15) 11 (7) 5 (3) 1 0

NC Lincoln Lincolnton, NC Crouse 371090004 0.072 25 (13) 10 (6) 1 1 0

NC Wake Raleigh-Cary, NC Fuquay-Varina 371830016 0.071 27 (19) 11 (8) 3 (2) 2 (2) 1

NC Rowan Salisbury, NC Rockwell 371590021 0.073 35 (21) 21 (13) 5 (4) 2 (1) 1

NC Rowan Salisbury, NC Enochville School 371590022 0.072 28 (17) 16 (8) 5 (3) 3 (2) 1

NC Forsyth Winston-Salem, NC 370670022 0.073 28 (14) 13 (7) 5 (3) 2 (2) 0

OH Ashtabula Ashtabula, OH CONNEAUT 390071001 0.075 26 (11) 12 (6) 5 (3) 4 (2) 2

OH Allen Lima, OH LIMA BATH 390030009 0.073 38 (25) 17 (14) 3 (3) 1 1

OH Knox Mount Vernon, OH CENTERBURG 390830002 0.073 22 (12) 6 (4) 4 (3) 1 1
165

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

OH Clark Springfield, OH SPRINGFIELD WELL FIELD 390230001 0.075 43 (23) 14 (7) 4 (3) 1 1

OH Clark Springfield, OH MUD RUN 390230003 0.073 34 (20) 11 (6) 3 (2) 1 1

OH Lucas Toledo, OH LOW_SER 390950034 0.073 22 (17) 15 (6) 5 (2) 2 (2) 1

OH Wood Toledo, OH BOWLING GREEN 391730003 0.071 26 (15) 9 (7) 3 (3) 1 1

OH Fayette Washington Court 

House, OH, AR Deer Creek 390479991 0.072 21 (10) 8 (4) 4 (2) 1 1

OH Jefferson Weirton-Steubenville, 

WV-OH STEUBEN 390810017 0.071 22 (17) 9 (6) 3 (2) 0 0

OK Sequoyah Fort Smith, AR-OK 401359021 0.072 30 (19) 10 (8) 3 (3) 2 (2) 0

OK Pittsburg McAlester, OK McALESTER MUNICIPAL AIRPORT 401210415 0.075 41 (25) 13 (8) 4 (2) 1 0

OK Cherokee Tahlequah, OK TAHLEQUAH SHELTER 400219002 0.074 37 (18) 16 (8) 5 (4) 0 0

PA Blair Altoona, PA 420130801 0.073 22 (14) 12 (9) 5 (4) 4 (3) 2 (2)

PA Clearfield DuBois, PA MOSHANNON STATE FOREST 420334000 0.071 13 (7) 2 (2) 2 (1) 1 1

PA Erie Erie, PA 420490003 0.074 26(18) 15(12) 8(6) 3(3) 1

PA Dauphin Harrisburg-Carlisle, PA A420431100LAT/LON POINT IS AT 

CORNER OF TRAILER 420431100 0.074 21(11) 9(5) 3(3) 1 0

PA Indiana Indiana, PA 420630004 0.075 31(17) 19(14) 13(9) 3(2) 1

PA Lancaster Lancaster, PA A420710007LAT/LON POINT AT 

CORNER OF TRAILER 420710007 0.075 29(16) 20(12) 9(6) 3(2) 1

PA Lancaster Lancaster, PA Lancaster DW 420710012 0.075 27(14) 16(10) 8(5) 5(4) 1

PA Lawrence New Castle, PA 420730015 0.073 18(11) 8(5) 5(4) 2(2) 0

PA Berks Reading, PA Reading Airport 420110011 0.073 24(12) 10(5) 3(2) 0 0

PA Centre State College, PA Penn State 420279991 0.072 15(10) 10(6) 4(2) 2(2) 0

PA York York-Hanover, PA York DW 421330011 0.074 28(16) 12(7) 6(3) 1 0

PA York York-Hanover, PA A421330008LAT/LON POINT AT 

CORNER OF TRAILER 421330008 0.072 23(13) 9(6) 3(2) 1 0
166

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

SC Spartanburg Spartanburg, SC NORTH SPARTANBURG FIRE STATION 

#2 (Shady Grove) 450830009 0.072 19(14) 8(6) 5(4) 2(1) 0

TN Sullivan Kingsport-Bristol-Bristol, 

TN-VA Blountville Ozone Monitor 471632002 0.071 18(11) 6(4) 3(3) 2(2) 1

TN Blount Knoxville, TN Great Smoky Mountains National 

Park, Look Rock 470090101 0.074 45(36) 16(12) 7(7) 3(3) 0

TN Jefferson Morristown, TN New Market ozone monitor 470890002 0.073 23(12) 8(5) 7(4) 3(3) 3(3)

TN Sevier Sevierville, TN 471550101 0.072 23(18) 11(9) 3(2) 1 0

TX Travis Austin-Round Rock, TX Austin Audubon Society 484530020 0.073 17(8) 5(4) 1 0 0

TX Travis Austin-Round Rock, TX Austin Northwest 484530014 0.072 25(17) 8(4) 4(3) 0 0

TX Jefferson Beaumont-Port Arthur, 

TX SETRPC 40 Sabine Pass 482450101 0.075 33(20) 18(12) 9(7) 5(3) 5(3)

TX Jefferson Beaumont-Port Arthur, 

TX Beaumont Downtown 482450009 0.072 19(12) 11(6) 2(1) 0 0

TX Jefferson Beaumont-Port Arthur, 

TX Hamshire 482450022 0.071 23(15) 8(4) 2(1) 1 1

TX Navarro Corsicana, TX Corsicana Airport 483491051 0.072 28(18) 8(3) 2(1) 1 0

TX El Paso El Paso, TX El Paso UTEP 481410037 0.072 26(11) 7(3) 1 0 0

TX Bell Killeen-Temple-Fort 

Hood, TX Killeen Skylark Field 480271047 0.074 30(15) 11(5) 2(1) 1 0

TX Harrison Marshall, TX Karnack 482030002 0.072 30(19) 9(7) 2(1) 0 0

TX Smith Tyler, TX Tyler Airport Relocated 484230007 0.075 36(21) 11(5) 4(3) 1 0

TX McLennan Waco, TX Waco Mazanec 483091037 0.074 29(20) 11(7) 4(2) 1 0

UT Weber Ogden-Clearfield, UT Harrisville 490571003 0.074 45(25) 11(7) 2(1) 1 0

UT Weber Ogden-Clearfield, UT Ogden 490570002 0.072 18(11) 7(4) 2(1) 1 0

UT Utah Provo-Orem, UT North Provo 490490002 0.073 21(11) 9(5) 2(1) 1 0
167

State County CBSA Monitor Site Name Monitor 

Site ID

Monitor 

Design 

Value 

(ppm)

Total 

days 

70+ ppb

(max/yr

)

Total 

days 

75+ ppb

(max/yr

)

Total 

days 

80+ 

ppb 

(max

/yr)

Total 

days 

85+ 

ppb 

(max

/yr)

Total 

days 

90+ 

ppb 

(max

/yr)

UT Washington St. George, UT Zion National Park, Dalton's Wash 490530130 0.072 23(12) 5(5) 1 0 0

VA Charles Richmond, VA Shirley Plantation 510360002 0.073 22(11) 13(6) 8(4) 5(3) 3(2)

VA Henrico Richmond, VA MathScience Innovation Center 510870014 0.073 26(15) 13(8) 5(3) 4(3) 2(2)

VA Hanover Richmond, VA Turner Property, Old Church 510850003 0.072 20(11) 9(4) 5(3) 2(2) 1

VA Caroline Richmond, VA USGS Geomagnetic Center, Corbin 510330001 0.071 15(10) 6(4) 2(1) 0 0

VA Hampton 

City

Virginia Beach-NorfolkNewport News, VA-NC NASA Langley Research Center 516500008 0.072 17(9) 7(4) 1 1 1

WV Kanawha Charleston, WV

CHARLESTON BAPTIST TEMPLE/SITE 

MOVED FROM OAQ AND FIRE 

STATION

540390010 0.073 30(17) 10(7) 5(4) 3(3) 3(3)

WV Hancock Weirton-Steubenville, 

WV-OH 540291004 0.072 26(16) 9(5) 5(3) 0 0

WI Outagamie Appleton, WI APPLETON AAL 550870009 0.072 20(13) 8(6) 3(3) 1 1

WI Dodge Beaver Dam, WI Horicon Wildlife Area 550270001 0.072 24(16) 10(8) 4(3) 1 1

WI Fond du Lac Fond du Lac, WI FOND DU LAC 550390006 0.072 22(15) 9(7) 4(3) 1 1

WI Kewaunee Green Bay, WI

JUMBOS DRIVE-IN PROPERTY, SOUTH 

END OF KEWAUNEE, 250' EAST OF 

HWY 42

550610002 0.074 20(14) 13(11) 6(5) 5(4) 3(2)

WI Walworth Whitewater, WI LAKE GENEVA 551270005 0.071 20(15) 8(7) 3(3) 2(2) 1
168

As discussed in above, given that it is clear that numerous days will have 8-hour average 

ozone concentrations at and well above the level of NAAQS in a single ozone season, EPA 

cannot rely on assuming that people, and especially children, will spend their time indoors to 

justify setting a higher ozone standard. EPA needs to ensure that the air is safe to breathe even—

and especially—if people elect to spend time outdoors. This is what the Clean Air Act promises. 

And this is what EPA should be encouraging. Limiting children’s opportunities to play outside 

by setting an unprotective NAAQS is unlawful and inconsistent with EPA’s duty under the Clean 

Air Act.

d. EPA’s Purported Justification for Its Preferred Form Is 

Arbitrary and Capricious

EPA’s claim that its preferred form somehow provides “stability” that enhances 

implementation is irrational. See Proposed Rule at 75,294/3-95/1. EPA appears to be concerned 

that meteorological conditions vary from year to year and “could have the effect of reducing 

public health protection, to the extent they result in frequent shifts in and out of attainment.” Id. 

at 75,294/2-3. 

EPA fails to explain why the 4th highest level will be any more stable than the 3rd, 2nd, 

or 1st highest levels. Although EPA purports to justify its decision to use the 4th highest form of 

the standard on the need for administrative stability, this need can be almost fully accomplished 

through use of a 1st or 2nd highest 3-year average. To evaluate EPA’s purported justification, we 

calculated “design values” for every CBSA for each 3-year period beginning with 2000-2002 

and ending with 2012-2014. The “design value” was calculated in three different ways: (a) using 

the 3-year average of 4th highest 8-hour daily maximums; (b) using the 3-year average of 1st 

highest 8-hour daily maximums; and (c) using the 3-year average of 2nd highest 8-hour daily 

maximums. We then calculated the year-to-year absolute value difference between design 

values using each of these three forms. The data are provided in Exhibit 12. The results show 

that the stability benefit of using a 4th highest as opposed to a 1st or 2nd highest form is marginal 

at best. Based on the data from 2000 to 2014, the average year-to-year change in design value 

using a 1st highest design value form is 3.2 ppb, as compared with 2.8 ppb for a 2nd and 2.5 ppb 

for a 4th highest form. These very modest differences in year-to-year design value changes fail to 

support EPA's purported administrative stability rationale.

EPA also fails to explain how “frequent shifts in and out of attainment” would reduce 

public health protection. Provided a nonattainment area retains its nonattainment designation 

(and does not seek a “clean data determination” (which is itself unlawful and arbitrary)), all 

control requirements remain in place even if that area has unusually low ozone levels. Thus, 

there would be no reduction in public health protection. For the other circumstance—an 

attainment area that shifts into nonattainment—EPA suggests no basis for concluding that there 

would somehow be less public health protection in effect. To the contrary, there would be a 

greater need for public health protection.

Finally, the statute and EPA’s past practice belie its explanation. EPA cannot redesignate 

a nonattainment area as attainment based on the area’s happening to have an unusually good 
169

year. 42 U.S.C. § 7407(d)(3)(E) (conditioning redesignation to attainment on, inter alia, “the 

improvement in air quality [being] due to permanent and enforceable reductions in emissions”). 

EPA’s unlawful and arbitrary clean data determinations must themselves be revoked when an 

area’s air quality deteriorates. E.g., 40 C.F.R. § 51.918. And, in the other direction, EPA 

arbitrarily and unlawfully virtually never redesignates attainment areas as nonattainment even 

when they consistently violate the ozone NAAQS. Thus, the form of the standard does not 

augment programmatic “stability.”

C. The Proposal Fails to Fully and Rationally Explain Reasons for Differing 

from CASAC’s Advice

Under the Act, EPA’s proposal must “set forth or summarize and provide a reference to 

any pertinent findings, recommendations, and comments by [CASAC],” and “if the proposal 

differs in any important respect from any of these recommendations,” must set forth “an 

explanation of the reasons for such differences.” 42 U.S.C. § 7607(d)(3). Thus, EPA “must fully 

explain” its reasons for any departure from CASAC’s recommendation. Mississippi v. EPA. 744 

F.3d 1334, 1354 (D.C. Cir. 2013). EPA must also provide such an explanation in the final rule. 

Id. 1355. 

Further, “EPA must be precise in describing the basis for its disagreement with CASAC. 

If EPA’s quarrel is with CASAC’s scientific analysis, then in order to preserve the integrity of 

CASAC’s scientific role, EPA must give a sound scientific reason for its disagreement.” Id. 

Here, EPA’s proposal fails to follow CASAC’s recommendations in a number of 

important respects, as further detailed below. In each case, the proposal does not meet the 

above-described requirements for providing a full and rational explanation for such failure. 

1. Primary Standard

a. Identification of Adverse Effects

CASAC expressly stated its view that “estimation of FEV1 decrements of >15% is 

appropriate as a scientifically relevant surrogate for adverse health outcomes in active healthy 

adults, whereas an FEV1 decrement of >10% is a scientifically relevant surrogate for adverse 

health outcomes for people with asthma and lung disease.”411 CASAC further found that lung 

function decrements greater than or equal to 15% in children “have been shown to result in 

significant adverse effects.”412 

EPA’s proposal fails to follow the foregoing advice from CASAC regarding what 

constitutes effects that are adverse, and fails to rationally explain why. Although EPA asserts that 

it considers the occurrence of ozone-induced FEV1 decrements > 10 and 15% as surrogates for 

 

411 CASAC Letter 2014a at 3.

412 Id. at 7; see also id. at 4 (stating that “[a]t the level of the current standard, 11% to 22% of school age children are 

predicted to experience at least one day with an FEV1 decrement >10%, which is not protective of public health.”); 

id. at 7 (citing “findings of adverse effects, including clinically significant lung function decrements and airway 

inflammation, after exposures to 60 ppb ozone in healthy adults”).).
170

occurrence of adverse health outcomes,413 its proposed decision arbitrarily refuses to treat such 

decrements as adverse. In actually deciding on options for the level of the standard, EPA 

repeatedly indicates that, as a practical matter, it does not consider adverse effects to be 

adequately shown unless: a) there is a finding of both lung function decrements and statistically 

significant increases in respiratory symptoms (compared to filtered air) in order to show 

adversity; or b) a showing of repeated occurrences of FEV decrements > 10 and 15%.414 Neither 

of these tests is consistent with CASAC’s recommendations. Nowhere did CASAC state that 

such lung function decrements needed to be accompanied by statistically significant respiratory 

symptoms in order for adverse effects to be shown. Further, as shown above, CASAC made clear 

that individual instances of lung function decrements > 10 and 15% are adequate surrogates by 

themselves for adverse effects: CASAC did not advise that multiple occurrences of such 

decrements were necessary to show adversity.415 

EPA fails to explain or rationally justify its employment of more demanding tests for 

adverse effects than recommended or employed by CASAC. The agency asserts that the ATS 

has identified the combination of lung function decrements and respiratory symptoms as adverse, 

but that is only one of a number of grounds established by ATS for identifying effects as adverse, 

and ATS has also identified adverse effects criteria that are clearly met in this case at levels of 70 

ppb and lower. For example, ATS has also identified as adverse “medically significant 

physiologic changes generally evidenced by” (among other things), use of medicine and 

“[i]nterference with the normal activity of the affected person or persons,”416 while EPA’s 2006 

Criteria Document (Table 8-3, p. 8-68) makes clear that for people with lung FEV1 decrements ≥ 

10% but < 20% would likely interfere with normal activities for many individuals, and would 

likely result in more frequent medication use. Likewise, in the 2008 ozone NAAQS, EPA itself 

said that a lung function decrement of ≥ 10% “represent[s] a level that should be considered 

 

413 Proposed Rule at at 75,306/1.

414 E.g. id. at 75,304/3, 75,305/1, 75,306/2. EPA’s proposal is at best equivocal even as to whether such repeated 

decrements qualify as adverse. The agency vaguely asserts that it “considers the extent to which a standard ...would 

be expected to protect the population from experiencing O3-induced FEV1 decrements >10% and >15% ...”, and 

that multiple such exposures “may” be considered to be adverse. Id. 75,306/2. Moreover, in describing the grounds 

for its proposed decisions (e.g., selection of the range of 65-70 ppb), EPA focuses on the combination of lung 

decrements and statistically significant respiratory symptoms as the benchmark for adverse effects, without treating 

lung decrements >10% or >15% as also determinative of adverse effects. E.g., id. at 75,304/2-3, 75,308/3-

75,309/1, 75,309/3. That is not consistent with CASAC’s advice. Rather, CASAC made clear its view that FEV1 

decrements >10% were scientifically relevant surrogates for adverse effects in persons with asthma and lung disease 

and decrements >15% were surrogates for adverse effects in healthy individuals. It did not state or suggest that such 

decrements merely “may” be considered adverse. CASAC further expressly described such effects as adverse or the

equivalent. CASAC Letter 2014a at 4 (ozone producing an FEV1 decrement >10% in children is not protective of 

public health.”); id. at 7 (describing as “adverse effects” clinically significant lung function decrements and airway 

inflammation); id. (finding that lung function decrements greater than or equal to 15% in children “have been shown 

to result in significant adverse effects”). EPA makes no attempt to explain why CASAC’s position on this score is 

wrong.

415 CASAC Letter 2014a at 3, 4, 7. To the extent EPA is suggesting that in determining adversity it is merely giving 

less weight to effects that do not meet its more demanding tests, that approach is also contrary to CASAC’s advice. 

CASAC nowhere qualified its advice that FEV1 decrements > 10% and >15% are adequate surrogates for adversity, 

nor did CASAC suggest that determination of adversity involved some sort of balancing or weighing of impacts. To 

the contrary, as noted above, CASAC expressly found that single occurrences of such decrements showed adverse 

effects. 

416 Proposed Rule at 75,263/1.
171

adverse for asthmatic individuals.”417 And in 2011, the CASAC Ozone Panel stated that 

“'[c]linically relevant effects are decrements >10%, a decrease in lung function considered 

clinically relevant by the American Thoracic Society.”

418 The CASAC Ozone Panel also stated 

that: [A] 10% decrement in FEV1 can lead to respiratory symptoms, especially in individuals 

with pre-existing pulmonary or cardiac disease. For example, people with chronic obstructive 

pulmonary disease have decreased ventilatory reserve (i.e., decreased baseline FEV1) such that a 

≥ 10% decrement could lead to moderate to severe respiratory symptoms.419 Yet EPA is now 

abandoning the FEV1>10% benchmark that CASAC, ATS and even EPA itself have all adopted 

without even an explanation as to how this sudden shift is even justified by the science. 

EPA also fails to rationally justify its view that single occurrences of FEV1 decrements >

10 and 15% are somehow of doubtful adversity. CASAC found that such single occurrences of 

such decrements do qualify as adverse and can endanger public health. ATS has further 

specifically identified exposure to air pollution that increases the risk of an adverse effect to the 

entire population as adverse, even though it may not increase the risk of any individual to an 

unacceptable level.420 EPA asserts that it “does not believe it would be appropriate to set a 

standard that is intended to eliminate all ozone-induced FEV1 decrements,” but that is different 

than FEV1 decrements >10%, and EPA asserts that this is consistent with CASAC’s advice, 

which did not include a recommendation to set the standard level low enough to eliminate all 

ozone-induced FEV1 decrements >10% or >15%.421 That bare assertion, however, simply does 

not address whether the referenced decrement levels are sufficient to connote adverse effects, 

and if not, why not. 

CASAC’s advice on this score is scientific in nature and quite clear: It refers to the 10% 

and 15% FEV1 decrement thresholds as “scientifically relevant” surrogates for adverse effects. 

Therefore, EPA would need to articulate sound scientific grounds for rejecting that advice. EPA 

has failed to do so. Even if CASAC’s advice were policy advice, EPA has offered no rational 

reason for departing from it.

b. Failure to Propose a Range of the Primary Standard that 

Includes Levels Down to 60 ppb

CASAC stated as one of its “scientific conclusions” the following:

The CASAC concurs that 60 ppb is an appropriate and justifiable scientifically based 

lower bound for a revised primary standard. This is based upon findings of adverse 

effects, including clinically significant lung function decrements and airway 

inflammation, after exposures to 60 ppb ozone in healthy adults with moderate exertion 

(Adams 2006; Schelegle et al., 2009; Brown et al. 2008; Kim et al., 2011), with limited 

evidence of adverse effects below 60 ppb. The CASAC further notes that clinical studies 

 

417 73 Fed. Reg. at 16,454/3-55/1.

418 Letter from CASAC Chair Dr. Jonathan M. Samet to U.S. EPA Administrator Lisa P. Jackson on CASAC 

Response to Charge Questions on the Reconsideration of the 2008 Ozone National Ambient Air Quality Standards, 

(EPA-CASAC-11-004), 2, Mar. 30, 2011

419 Id. at 7. 

420 Proposed Rule at 75,263/1. 

421 Id. 
172

do not address sensitive subgroups, such as children with asthma, and that there is a 

scientific basis to anticipate that the adverse effects for such subgroups are likely to be 

more significant at 60 ppb than for healthy adults.422

The above statement appeared in a portion of the CASAC letter specifically identified by 

CASAC as providing scientific conclusions.423

 

Contrary to the above-quoted scientific advice from CASAC, EPA did not set 60 ppb as 

the lower bound for its proposed range for the primary standard. EPA fails to offer sound 

scientific reasons for rejection of CASAC’s advice on this score. Instead, EPA relies on various 

assertions of alleged uncertainties and policy concerns.424 Indeed, in a key paragraphs that seeks 

to justify rejection of CASAC’s recommendation of 60 ppb as the lower bound, EPA recites 

claims of “uncertainty” no less than seven times. Yet the D.C. Circuit has ruled that assertions of 

uncertainty do not suffice to explain rejection of CASAC’s scientific conclusions. Mississippi, 

744 F.3d at 1357. EPA must explain why the evidence on which CASAC relied cannot support 

the degree of confidence CASAC placed in it. Id. EPA fails to do so here. The only 

explanations EPA offers on this score lack sound scientific support, are arbitrary, and/or are 

based on policy concerns. 

For example, EPA asserts that a decision to set the primary standard at 60 ppb “would 

place a large amount of weight on the potential public health importance of virtually eliminating 

even single occurrences of exposures of concern at and above 60 ppb, though controlled human 

exposure studies have not reported the adverse combination of respiratory symptoms and 

decrements in lung function following exposures to 60 ppb.”425 This explanation:

 Fails to confront CASAC’s stated rationale: namely, the “findings of adverse 

effects, including clinically significant lung function decrements and airway 

inflammation, after exposures to 60 ppb ozone in healthy adults.” CASAC did 

not find that its recommendation of 60 as the low end of the range required 

placing a large amount weight on virtually eliminating single exposures above 60 

(although such single exposures would plainly meet CASAC’s definition of 

adverse effects as discussed above). To the contrary, CASAC noted that a 60 ppb 

standard would “reduce” such single exposures, and allow virtually no children to 

experience “two or more exposures in a year.” 426

 Supplants CASAC’s, ATS’s, and even EPA’s assessment of what constitutes an 

adverse health effect—FEV1 10% or greater decrements--with EPA’s new 

requirement to that there be a combination of respiratory symptoms and lung 

decrements. Indeed, EPA takes this a step further by attempting to ascribe 

significance to the alleged absence of exposure studies finding the combination of 

 

422 CASAC Letter 2014a at 7. 

423 Id. at 6 (“While uncertainty is inherent in assessments of this type, CASAC finds that there is sufficient weight of 

evidence and degree of confidence to reach the following scientific conclusions”). 

424 Proposed Rule at 75,309/3. 

425 Id. 

426 CASAC Letter 2014a at 7 (emphasis added).
173

respiratory symptoms and lung decrements following 60 ppb exposures, but as 

the discussion above shows, EPA has failed to rationally explain why such a 

combination is necessary to show adversity of effects.

 Ignores whether the air is in fact save to breath by substituting an analysis of 

exposures to ozone with the required analysis of what level of ozone is in fact 

safe to breathe. 

EPA likewise asserts that setting the primary standard at 60 ppb would place a large 

amount of weight on the potential public health importance of further reducing the occurrence of 

ozone-induced lung function decrements > 10 and 15%.427 Again, this rationale is not responsive 

to CASAC’s reasoning, which: a) found the presence of adverse effects in healthy adults at 60 

ppb and identified not only lung function decrements, but lung inflammation as the bases for 

such finding, and b) found a scientific basis to anticipate that the adverse effects for sensitive 

subgroups are likely to be more significant at 60 ppb than for healthy adults. EPA offers no 

scientific bases for questioning any of these findings. The “potential public health importance” 

of further reducing lung function decrements is a policy consideration, not a refutation of 

CASAC’s scientific findings. In any event, EPA fails to rationally explain why further reducing 

the occurrence of ozone-induced lung function decrements > 10 and 15% is not of public health 

importance. EPA agrees that such decrements are surrogates for the occurrence of adverse 

health outcomes.428 As CASAC has found, and EPA does not dispute, lung function decrements 

greater than or equal to 15% in children “have been shown to result in significant adverse 

effects.” It is therefore irrational to suggest that reducing the occurrence of such decrements is 

somehow not of public health importance and direct legal relevance under the Clean Air Act. 

EPA asserts that not every occurrence of an ozone-induced FEV1 decrement will be adverse, but 

the agency itself concedes that single occurrences of such decrements can potentially result in 

adverse effects, and repeated occurrences may be considered adverse even in healthy adults.429 

And the agency’s own risk assessment shows that the number of children expected to suffer such 

decrements is hardly trivial. For example, in just the 15 cities studied, the HREA estimates that 

122,000 more asthmatic children would suffer at least one decrement > 10% at 70 ppb ozone 

than at 60 ppb.430 And 337,000 more children would suffer at least one decrement > 15% at 70 

ppb than at 60.431 Likewise, the HREA estimates that in the case study cities alone, 72,000 more 

asthmatic children will suffer two or more decrements > 10% at 70 ppb ozone than at 60 ppb.432 

And 175,000 more children would suffer two or more decrements > 15% at 70 ppb ozone than at 

60 ppb.433 The numbers suffering such exposures would obviously be much greater nationally. 

EPA does not and cannot explain why impacts of such magnitude are not a public health concern 

in the setting the NAAQS. Indeed, EPA says that it agrees with CASAC on the importance of 

limiting exposures to O3 concentrations as low as 60 ppb.434 

 

427 Proposed Rule at 75,309/3. 

428 Id. 75,306/1. 

429 Id. 75,306/2. 

430 Id. at 75,275. 

431 Id. 

432 Id. 

433 Id. 

434 Id. at 75,310. 
174

EPA also asserts that setting the primary standard at 60 ppb would place a large amount 

of weight: a) on analyses of ambient ozone concentrations in locations of multicity 

epidemiologic studies, despite alleged uncertainties in linking multicity effect estimates for 

short-term ozone with air quality in individual study cities; and b) on epidemiology-based risk 

estimates, despite allegedly important uncertainties in those estimates. EPA’s refusal to give 

serious weight to the multicity studies and epidemiology-based risk estimates in determining the 

level of the standard is arbitrary for reasons discussed elsewhere in these comments, incorporated 

by reference here.435 In any event, CASAC did not say it was placing “a large amount of weight” 

on such studies and estimates in recommending a lower bound of 60 ppb. It said only that a 60 

ppb standard ‘would be expected to reduce epidemiology-based mortality and morbidity risk for 

short-term exposures to ozone,” and cited that fact as only one among a number of grounds 

supporting such a level as a lower bound.436 Further, it is arbitrary for EPA to contend that 

alleged uncertainties in the epidemiology-based risk estimates are so great that it is not 

appropriate to use them at all to support the appropriateness of standard levels below 65 ppb.437 

Neither the ISA nor the PA take such an extreme position, nor does the record support it. Nor 

did CASAC, and EPA has failed to justify its departure from CASAC on this point. Moreover, 

EPA fails to provide a reasoned basis for using these risk estimates to support consideration of 

standard levels of 70 and 65, but not 60: There is no reasoned explanation for concluding that 

uncertainties in those estimates become so much greater at 60 ppb than at 65 ppb that EPA is 

justified in ignoring them entirely in considering a 60 ppb standard.

Similarly, EPA’s assertions that CASAC’s recommendation of a lower bound of 60 ppb 

placed “a large amount of weight” on specific factors as noted above is further belied by 

CASAC’s explicit statement that its recommendation of a range of 60-70 ppb was based on the 

entire body of scientific evidence: 

The CASAC further concludes that there is adequate scientific evidence to recommend a 

range of levels for a revised primary ozone standard from 70 ppb to 60 ppb. The CASAC 

reached this conclusion based on the scientific evidence from clinical studies, epidemiologic 

studies, and animal toxicology studies, as summarized in the Integrated Science Assessment 

(ISA), the findings from the exposure and risk assessments as summarized in the HREA, and

the interpretation of the implications of these sources of information as given in the Second 

Draft PA.

438

Thus, EPA’s stated reasons for rejecting CASAC’s recommendations are based on the false 

premise that CASAC placed a large amount of weight on the individual factors EPA cites, when 

in reality CASAC relied on the evidence collectively.

EPA further asserts that because not all exposures of concern lead to adverse effects and 

the NAAQS are not meant to be zero-risk or background standards, “alternative standard levels 

 

435 EPA cites “particularly uncertainties in the shape of the concentration-response functions at lower O3 

concentrations,” Id. at 75,309/3, but in so finding, the ISA and Policy Assessment were referring to ozone levels 

below 60 ppb. See, e.g., 3-64, 3-115-16. 

436 CASAC Letter 2014a at 7.

437 Proposed Rule at 75,309/3. 

438 CASAC Letter 2014a at ii (emphasis added); see also id. at 8. 
175

below 65 ppb are not needed to further reduce such exposures.”439 That claim misstates 

CASAC’s rationale and is arbitrary. CASAC did not claim that all exposures of concern lead to 

adverse effects, nor did it advocate zero-risk or background standards: Instead, it cited the range 

of evidence showing the likelihood of adverse effects at 60 ppb, and EPA’s own risk assessment 

that a substantial number of children suffer such effects at levels at and above 60 ppb. 

Moreover, it is a non-sequitur for EPA to equate 60 ppb with a “zero-risk” or “background” 

standard. As EPA’s own findings show, even at 60 ppb, substantial numbers of children would 

suffer lung decrements that EPA agrees are surrogates for adverse effects, so 60 is plainly not 

zero risk. And EPA’s analysis in this rulemaking shows that 60 ppb is far above average (and 

most maximum) U.S. background levels. 

* Finally, EPA’s uncertainty claims simply fail to address the strength of the exposure 

studies that show adverse lung decrements as well as inflammation at 60 ppb. See part V.B.1.b 

above. CASAC justifiably relied on these studies in recommending 60 ppb as the low end of the 

range, and EPA fails to offer any reasoned justification for questioning that reliance. That failure 

is especially telling given that EPA purports to give the greatest weight to the exposure studies in 

determining the level of the NAAQS.

For all of the above reasons, EPA acted arbitrarily and failed to articulate a sound 

scientific basis for rejecting CASAC’s recommendation that 60 ppb be considered as a level of 

the standard.

c. EPA’s Inclusion of 70 ppb in the Proposed Range

Although CASAC recommended a range of 60 to 70 ppb for the primary standard, it also 

made scientific findings that adverse effects are likely at, and below,70 ppb. Specifically, 

CASAC found that “[a]t 70 ppb, there is substantial scientific certainty of a variety of adverse 

effects, including decrease in lung function, increase in respiratory symptoms, and increase in 

airway inflammation.” CASAC Ltr. 8 (emphasis added). CASAC reiterated and supported that 

finding elsewhere in its letter to the Administrator. See id. at 6 (“The 70 ppb-8hr benchmark 

level reflects the fact that in healthy subjects, decreases in lung function and respiratory 

symptoms occur at concentrations as low as 72 ppb and that these effects almost certainly occur 

in some people, including asthmatics and others with low lung function who are less tolerant of 

such effects, at levels of 70 ppb and below)(emphasis added); id. at 7 (“At a level of 70 ppb for 

the averaging time and form of the current standard, clinical and epidemiological studies show 

adverse effects to human health); id (HREA findings “indicate that ozone exposures of 70 ppb 

...are of significant concern, especially for children, asthmatics, the elderly and other at risk 

populations”).

EPA’s proposal of a range for the primary standard that includes 70 ppb cannot be 

squared with the above-quoted CASAC findings. The primary standard must “be set at a level at 

which there is ‘an absence of adverse effect’ on [] sensitive individuals” such as children, the 

elderly, and people with respiratory illnesses. Lead Indus. Ass’n v. EPA, 647 F.2d 1130, 1153 

(D.C. Cir. 1980). Because CASAC found substantial scientific certainty of adverse effects at 70 

ppb, and found the adverse combination of decrements and respiratory symptoms is almost 

 

439 Proposed Rule at 75,301/1. 
176

certain to occur at and below 70 ppb, EPA must set the standard below 70 ppb to assure the 

absence of adverse effects, unless EPA articulates sound scientific reasons for rejecting 

CASAC’s findings on this score. Mississippi, 744 F.3d at 1355 (“If EPA’s quarrel is with 

CASAC’s scientific analysis, then ...EPA must give a sound scientific reason for its 

disagreement”); Am. Trucking Ass’ns, 283 F.3d at 378-79 (The Act “require[s] that EPA must 

either follow CASAC‟s advice or explain why the proposed rule „differs . . . from . . . 

[CASAC‟s] recommendations‟”)(citations omitted, alterations in original). 

EPA’s proposal does not even attempt to articulate scientific grounds for rejecting the 

above-quoted CASAC findings. EPA notes CASAC’s statement that EPA’s choice of a level 

within the 60-70 ppb range is a policy judgment, but that hardly converts the above-quoted 

scientific findings into policy judgments. The D.C. Circuit has made clear that where CASAC 

makes a scientific finding that adverse effects are likely at a given ozone level, EPA must either 

act in accord with that finding or articulate sound scientific reasons for disagreeing therewith. 

Mississippi, 744 F.3d at 1355, 1357-58; Am. Trucking Ass’ns, 283 F.3d at 378-79. Further, even 

if CASAC’s advice on this score were purely a policy recommendation, EPA must still provide a 

rational, non-arbitary basis for rejecting it. Id.1355. As discussed above and elsewhere in these 

comments, EPA has failed to provide such a basis. Indeed, EPA’s own staff found that effects 

EPA agrees are adverse are likely at levels of 70 ppb and below (“Thus, respiratory symptoms 

combined with lung function decrements are likely to occur to some degree in healthy adults 

with 6.6-hour exposures to concentrations below 70 ppb, and are more likely to occur with 8-

hour exposures to 70 ppb and below”).440 

EPA does note a CASAC statement, in the context of the adequacy of the current 

NAAQS, that the adverse combination of lung function decrements and respiratory symptoms 

almost certainly occurs in some people following exposures to ozone concentrations lower than 

72 ppb – the level at which such adverse combination was shown in the exposure study by 

Schelegle et al. (2009).441 EPA goes on to state: “Though CASAC did not provide advice as to 

how far below 72 ppb adverse effects would likely occur, the Administrator agrees that such 

effects could occur following exposures at least somewhat below 72 ppb.”442 EPA is simply 

incorrect in claiming that CASAC “did not provide advice as to how far below 72 ppb adverse 

effects would likely occur.” As noted above, CASAC expressly found that there is substantial 

scientific certainty of adverse effects at 70 ppb, and that adverse effects are almost certain to 

occur at levels below 70 ppb as well.

443 CASAC makes clear throughout its comments that 

concentrations down to 60 ppb “result in lung function decrements large enough to be judged an 

abnormal response by ATS and that could be adverse in individuals with lung disease” and that a 

standard set at a level of 70 ppb is still of “of significant concern.”444

 

440 Policy Assessment at 4-11.

441 Proposed Rule at 75305/1, citing CASAC Letter 2014a at 5. 

442 Id. 

443 Although not directed at CASAC’s findings, EPA does assert at one point that the Administrator “has decreasing 

confidence that adverse effects will occur following exposures to O3 concentrations below 72 ppb.” Id. 75,305/2. 

But in the next sentence EPA goes on to say: “In particular, compared to O3 exposure concentrations at or above 72 

ppb, she has less confidence that adverse effects will occur following exposures to O3 concentrations as low as 60 

ppb.” id. at75305/2-75306/1. EPA thus says nothing there to dispute CASAC’s finding at 70 ppb.

444

 CASAC Letter 2014a at 7.
177

D. EPA Has Failed To Explain How It Has Accounted For A Margin Of Safety 

and Has Failed To Rationally Explain How The Standards It Has Proposed 

Incorporate A Margin Of Safety That Is Adequate

1. EPA Must Set Standards Requisite To Protect The Public Health And 

Provide For An Adequate Margin Of Safety

As discussed above, EPA is required to set primary standards that protect public health 

with an adequate margin of safety. 42 U.S.C. § 7409. This requirement is intended to address 

uncertainties associated with inconclusive scientific and technical information. It is also intended 

to provide a reasonable degree of protection against hazards that research has not yet identified.

State of Mississippi v. EPA, 744 F.3d 1334, 1353 (D.C. Cir. 2012).

The uncertainties to be addressed by the margin of safety are “components of the risk 

associated with pollution at levels below those at which human health effects can be said to 

occur with reasonable scientific certainty.”445 By requiring an adequate margin of safety, 

“Congress was directing EPA to build a buffer to protect against uncertain and unknown dangers 

to human health.” State of Mississippi, 744 F.3d at 1353.

A public health standard must be set at “the maximum permissible ambient air level . . . 

which will protect the health of any [sensitive] group of the population.”446 Thus, the primary 

standards must be set at a level that protects against adverse health effects in sensitive persons.

See generally Coal. Of Battery Recyclers Ass’n v. EPA, 604 F.3d 613, 618 (D.C. Cir. 2010).

Importantly, the standards must also provide an adequate margin of safety for vulnerable 

subpopulations. Am. Farm Bureau Fed’n, 559 F.3d at 525-26.

2. EPA’s Claim that Its Proposal Provides for an Adequate Margin of 

Safety Is Arbitrary and Capricious

EPA has arbitrarily and capriciously failed to show how its proposed range of 65-70 ppb 

provides an adequate margin of safety, for EPA fails to give appropriate consideration to key 

aspects of the margin of safety inquiry, such as how pollution thresholds might impact sensitive 

sub-populations. Am. Farm Bureau Fed’n, 559 F.3d.

As discussed above, CASAC has unequivocally concluded that there are adverse impacts 

at a 70 ppb level, using CASAC’s, ATS’s, and even EPA’s own definitions of what constitutes 

an adverse impact.447 Again, CASAC advised the following:

 

445 Proposed Rule at 75,238

446 Id. at 75,237 (referencing S. Rep. No. 91-1196, 91st Cong. 2d Sess. 10 (1970)).

447See CASAC Letter 2014a; Policy Assessment at ES-5 (stating a “standard set within this range would result in 

important improvements in public protection, compared to the current standard, and could reasonably be judged to 

provide an appropriate degree of public health protection, including for at-risk populations and lifestages.”)
178

At 70 ppb, there is substantial scientific evidence of adverse effects as detailed in 

the charge question responses, including decrease in lung function, increase in 

respiratory symptoms, and increase in airway inflammation...448

CASAC reiterated its scientific conclusion that there are adverse impacts at 70 ppb. 

The 70 ppb-8hr benchmark level reflects the fact that in healthy subjects, 

decreases in lung function and respiratory symptoms occur at concentrations as 

low as 72 ppb and that these effects almost certainly occur in some people, 

including asthmatics and others with low lung function who are less tolerant of 

such effects, at levels of 70 ppb and below)...449 

At a level of 70 ppb for the averaging time and form of the current standard, 

clinical and epidemiological studies show adverse effects to human health ozone 

exposures of 70 ppb...are of significant concern, especially for children, 

asthmatics, the elderly and other at risk populations.

450

And EPA staff conclusions are consistent with CASAC’s determination thatadverse effects are 

likely at even lower concentrations of ozone if the 8-hour averaging period used in the standard is 

applied.451

Nonetheless, EPA’s proposal includes consideration of a standard of 70 ppb. Even if this 

could be reconciled with the health studies of where significant adverse health impacts will 

occur—which it cannot—it makes it absolutely clear that at 70 ppb there is no margin of safety 

built into a 70ppb standard. With its proposal, EPA cannot reasonably assert that it has built a 

buffer that protects against uncertain and unknown danger posed to human health by ozone 

exposures.

Indeed, EPA agrees with CASAC “on the importance of limiting exposures to O3 

concentrations as low as 60 ppb,” and “recognizes that levels as low as 60 ppb could potentially 

be supported.”452 Setting a standard of 70 and asserting that it incorporates an adequate margin 

of safety is irreconcilable with EPA’s conclusion that it is important to limit exposures to 60 ppb 

and that the evidence in the record could justify a level of 60 ppb given the adverse impacts 

observed at levels above 60 ppb.

Further, contrary to EPA assertions, CASAC did not conclude that setting the health 

standard at 60 ppb would equate to the establishment of a zero-risk primary NAAQS. CASAC 

concluded the exact opposite—adverse health impacts were seen at 60 ppb in controlled human 

studies, just not below:

 

448 CASAC Letter 2014a at 8 (emphasis added). 

449 Id. at 6. 

450 Id. at 7.

451 Policy Assessment at 4-56; see also CASAC Letter 2014a at 5, (“It is the judgment of CASAC that if subjects 

had been exposed to ozone using the 8-hour averaging period used in the standard, adverse effects could have 

occurred at [a] lower concentration. Further, in our judgment, the level at which adverse effects might be observed 

would likely be lower for more sensitive subgroups, such as those with asthma.”)

452 Proposed Rule at 75,310.
179

The CASAC concurs that 60 ppb is an appropriate and justifiable scientifically 

based lower bound for a revised primary standard. This is based upon findings of 

adverse effects, including clinically significant lung function decrements and 

airway inflammation, after exposures to 60 ppb ozone in health adults with 

moderate exertion...with limited evidence of adverse effects below 60 ppb.

453

Again, this indicates that a standard of 70 ppb cannot be reconciled with protecting the public 

health, and certainly not with providing an adequate margin of safety. 

EPA’s own staff has found substantial evidence supporting ozone standard levels lower 

than the 65-70 ppb that the agency has proposed:

[T]he evidence from controlled human exposure studies supports considering 

alternative O3 standards levels at least as low as 60 ppb. Potentially adverse lung 

function decrements and pulmonary inflammation have been demonstrated to 

occur in healthy adults at 60 ppb. Thus, 60 ppb is a short-term exposure 

concentration that may be reasonably concluded to elicit adverse effect in at-risk 

groups. Pulmonary inflammation, particularly if experienced repeatedly, provides 

a mechanism by which O3 may cause other more serious respiratory morbidity 

effects (e.g. asthma exacerbations) and possibly extrapulmonary effects . . . [T]he 

physiological effects reported in controlled human exposure studies down to 60 

ppb O3 have been linked to aggravation of asthma and increased susceptibility to 

respiratory infection, potentially leading to increased medication use, increased 

school and work absences, increased visits to doctors’ offices and emergency 

departments, and increased hospital admissions.454

EPA has failed to rationally explain why an ozone standard level in the range of 65 ppb 

to 70 ppb would provide an adequate margin of safety (much less protect the public outright) 

when EPA’s staff has found that 60 ppb “may be reasonably concluded to elicit adverse effect in 

at-risk groups,” and when there is substantial evidence supporting that finding. EPA must 

reconsider its decision to disregard the recommendations given to it by CASAC and EPA staff.

3. EPA Has Failed to Rationally Explain How the Standards It Has 

Proposed Incorporate an Adequate Margin of Safety

EPA can choose reasonable means to provide an adequate margin of safety, but it must 

also fully and rationally explain how it did so, why it believes the proposed standard will provide 

an adequate margin of safety, and “why [the agency] chose one method rather than another” for 

ensuring the margin of safety. Am. Farm Bureau, 559 F.3d at 526; Am. Trucking Ass’ns v. EPA, 

283 F.3d 355, 368 (D.C. Cir. 2002); Lead Indus. Assn’n v. EPA, 647 F.3d 1130, 1161-1162 (D.C. 

Cir. 1980). EPA has failed to provide such an explanation here. EPA asserts that “it takes the 

need for an adequate margin of safety into account as an integral part of [its] decisionmaking on 

 

453 CASAC Letter 2014a at 7 (citations omitted) (emphasis added).

454 Policy Assessment at 4-57.
180

the appropriate level, averaging time, form, and indicator of the standard.”455 But nowhere does 

the agency explain: a) how and where the margin of safety requirement was factored into EPA’s 

decisionmaking on these matters in the proposal at issue here; b) why specifically EPA believes 

its decisions on these matters will ensure an adequate margin of safety; and c) why EPA chose 

the described method for meeting the margin of safety requirement as opposed to another 

approach (e.g., an approach whereby EPA adds the margin of safety after determining a level of 

likely adverse effects). EPA offers only bare assertions that its proposal provides for a margin a 

safety – assertions that fall far short of providing the above-described explanations as required by 

the statute, case law, and requirements for reasoned decisionmaking. 

EPA’s cursory background discussion456 of factors relevant to the margin of safety 

plainly does not suffice as an explanation of how the agency provided for a margin of safety in 

this specific case, and why it was sufficient. See Missouri Public Serv. Comm’n v. FERC, 601 

F.3d 581, 586 (D.C. Cir. 2010) (“a passing reference to relevant factors...is not sufficient to 

satisfy the [agency’s] obligation to carry out reasoned and principled decisionmaking.” (internal 

quotation marks omitted; second alteration in original)). Merely stating the governing legal or 

factual test is no substitute for applying that test to the record before the agency. Douglas Foods 

Corp. v. NLRB, 251 F.3d 1056, 1066 (D.C. Cir. 2001) (“The NLRB cannot discharge its 

obligation [to carry out an analysis of three factors and to weigh them] merely by citing the 

appropriate authority and averring that it gave proper consideration. It actually must consider the 

factors as they apply to the instant case, and explain the basis for its conclusions.”). In context of 

the Act’s health standards, EPA has the “heaviest of obligations to explain and expose every step 

of its reasoning.” American Lung Ass’n v. EPA, 134 F.3d 388, 392 (D.C. Cir. 1998). Deference 

to EPA’s expert judgment requires that the agency carefully and clearly explain exactly how it 

reached the result it did. Id. EPA has failed to provide such a clear explanation here. 

The mere fact that EPA has considered ozone’s effects on sensitive subpopulations does 

not by itself adequately explain how EPA’s proposal will actually assure an adequate margin of 

safety. Indeed, nowhere does EPA state that its consideration of ozone’s effects on sensitive 

populations is meant to address the margin of safety requirement. Nor does EPA explain how it 

is establishing a margin of safety for sensitive subpopulations. Acknowledging that these 

sensitive subpopulations exist and are more likely to suffer adverse effects at various ozone 

levels does not equate to explaining how or why the proposed standard will provide them with an 

adequate margin of safety.

Nor is it sufficient for EPA to simply assert that it takes the need for an adequate margin 

of safety into account as “an integral part of [its] decisionmaking on the appropriate level, 

averaging time, form, and indicator of the standard.”457 Such an assertion does not explain how 

or why such decisionmaking adequately addresses the margin of safety requirement. For 

example, nowhere does EPA explain how margin of safety considerations were integrated into its 

proposal on the form of the standard: Such integration is hardly apparent from the face of the 

proposed form, which – as discussed in part V.B.3. above – allows multiple exposures far in 

excess of levels in the 60-70 ppb range and an unlimited number of 8-hour periods in a given 

 

455 Proposed Rule at 75,309/1.

456 E.g., id. at 75,237-38, 75,304, n.157, 75,309.

457 Id. at 75,309
181

year in which people can be exposed to ozone levels higher than those at which EPA says 

adverse effects are likely to occur. Nor does EPA explain how margin of safety considerations 

were integrated into its proposal on the level of the standard. Among other things, as further 

discussed below and elsewhere in these comments, EPA fails to explain how its proposed range 

assures the absence of adverse effects to sensitive populations, much less provides such 

populations with an adequate margin of safety. Indeed, in determining the level of the proposed 

standard, EPA’s proposal repeatedly opts for a direction contrary to a key purpose of the margin 

of safety – namely, to build a buffer to protect against uncertain and unknown dangers to human 

health. For example, faced with evidence of adverse effects from ozone exposures in the 60-65 

ppb range, EPA – citing alleged uncertainties - refuses to even consider preventing such 

exposures.

458 Likewise, in proposing 70 ppb as the upper end of its range, EPA provides no 

buffer at all against adverse effects that CASAC found to be certain at 70 ppb with substantial 

scientific certainty. Nor does EPA respond at all to CASAC’s specific advice to set the standard 

below 70 ppb to provide an adequate margin of safety -- other than to assert that the choice 

involves a policy judgment. 

EPA’s failure to provide an explanation of how it is providing for the margin of safety 

here contrasts sharply with the agency’s actions in other NAAQS decisions, where the agency 

did provide such explanations. For example, in its 1979 ozone NAAQS decision, EPA 

“determined...the ‘probable level for adverse effects in sensitive persons,’” and then provided a 

margin of safety below that level based on a detailed consideration of multiple factors. Am. 

Petroleum Inst. v. Costle, 665 F.2d 1176, 1187 (D.C. Cir.1981) (citing 44 Fed. Reg. 8202, 8216-

17 (1979)). Here, in contrast, EPA does not identify a probable level for adverse effects in 

sensitive persons, much less explain how its proposed standard range provides a margin of safety 

below that level. In Lead Industries, rather than find an adverse effect level, then add a margin of 

safety, EPA incorporated the margin of safety at two places in the standard-setting process. 647 

F.2d at 1161-62 & n.80. EPA explained “why [it] chose one method rather than another” of 

providing a margin of safety, id. 1162, and explained in the rule itself the points at which it was 

accounting for margin of safety and how it was doing so, id. 1144. Thus, there are plainly ways 

for EPA to lay out how it is adequately addressing the margin of safety, including for sensitive 

subpopulations. 

EPA’s failure to explain itself on these issues is crucial because it goes to the heart of the 

agency’s duty in setting the NAAQS. Without a reasoned explanation, the public and reviewing 

courts cannot know whether EPA designed the standard to protect against not only known 

adverse effects on health, but those of scientific uncertainty. 

For all the foregoing reasons, EPA has failed to adequately explain how its proposal 

assures an adequate margin of safety as required by the Act.

E. Even if EPA Declines to Deviate from Its Proposed Range, EPA Must Set the 

Standard No Higher than 65 ppb, at the Bottom of Its Proposed Range 

As explained above, to fulfill its obligation under the Clean Air Act and to act rationally, 

EPA must set the NAAQS at 60 ppb. If EPA refuses to adopt a standard below its proposed 

 

458 Id. at 75,309-10. 
182

range of 65-70 ppb, however, it must set the standard at 65 ppb, for that will be closest to the 

requisite level. In no event should EPA set the standard as high as 70 ppb. We do not accept 

EPA’s reasoning for rejecting a level of 60 ppb, but on this basis, a standard of 65 ppb would 

better meet EPA’s stated criteria and provide significantly more protection.

The information before EPA shows that a standard of 65 ppb would prevent substantial 

incidents of adverse effects that are likely to occur at 70 ppb and would be significantly more 

protective than a standard of 70 ppb. EPA rejects a standard of 60 ppb, saying it “focuses on” 

and “emphasizes” limiting multiple exposures of concern to ozone and “balances” that focus 

against three factors: (1) the fact that “not all exposures of concern will result in adverse effects”; 

(2) a decreased confidence that adverse effects will occur at 60 ppb as opposed to at 70 or 80 

ppb; and (3) the belief that “NAAQS are not meant to be zero-risk standards.”459

As an initial matter, the balance EPA proposes is itself without foundation. As discussed 

elsewhere in these comments, a focus or emphasis on multiple exposures fails to assure the 

absence of adverse effects, as the evidence shows (and EPA concedes) that single exposures can 

and do produce adverse effects, both at the individual and population levels. For the same 

reasons, it is irrelevant that not all exposures of concern will result in adverse effects: The Act 

requires the standard to assure the absence of adverse effects in all groups, including sensitive 

populations, a mandate that is not met merely because some individuals or portions of the 

population do not suffer adverse effects from single or even multiple exposures to a given ozone 

level. Further, for the reasons given above, it is very likely that exposure to ozone at 60 ppb 

causes adverse effects in sensitive populations; EPA’s second countervailing factor is thus 

incorrect. EPA’s third countervailing factor rests on false premises. EPA cites Mississippi, 744 

F.3d at 1343, for the proposition that “NAAQS are not meant to be zero-risk standards.” 

Proposed Rule at 75,305/3 & n.163. That case does not establish the 

proposition. Mississippi says only, “Determining what is ‘requisite’ to protect the ‘public health’ 

with an ‘adequate’ margin of safety may indeed require a contextual assessment of acceptable 

risk.” 744 F.3d at 1343 (quoting Whitman, 531 U.S. at 494-95 (Breyer, J., concurring in part and 

concurring in the judgment)). The “may” indicates that the statement is just dicta. The underlying 

Supreme Court concurring opinion does not have the force of law, either: it is one Justice’s 

opinion that was not joined by any other member of the Court. In any event, the concern over 

“zero-risk standards” is misguided, for the issue here is whether EPA may set standards that 

allow large-scale, known adverse effects to persist. It may not.

Even if EPA’s “focus,” “emphasis,” and countervailing factors were valid (which we do 

not accept), they support a standard at least as protective as 65 ppb. Again, as discussed above, 

EPA cannot rely on assertions that exposures will not happen because people will stay inside and 

will not experience the unsafe ozone events that empirical evidence makes clear will in fact 

occur all around them. Nor in any event is the exposure study defensible. But even beyond 

these points, EPA’s own analysis makes clear that setting the standard at levels below 70 ppb 

reduces what even EPA acknowledges are multiple exposures to levels of pollution that CASAC 

has judged to cause adverse health impacts. 

 

459 Id. at 75,305/3.
183

For example, EPA finds that a level of 70 ppb would “virtually eliminate the occurrence 

of two or more O3 exposures of concern for the 70 and 80 ppb benchmarks, and ... substantially 

reduce the occurrence of two or more O3 exposures of concern for the 60 ppb benchmark, 

compared to the current standard” approximately a 60% reduction from the current standard.460

Again, as noted above, CASAC has concluded that the health science reflects adverse impacts at 

60 ppb and above. In contrast, a level of 65 ppb would be much more effective at eliminating 

these exposures, in fact it would “eliminate[ed] almost all exposures of concern” to the 

benchmarks of 70 and 80 ppb and “protect[ing] more than 99% of children in urban study areas” 

from multiple exposures to the benchmark of 60 ppb. For the 60 ppb benchmark, that protection 

would be approximately a 95% reduction from the current standard.461 For the 15 areas studied, a 

70 ppb standard would likely force 253,000 more kids to endure multiple exposures to at least 60 

ppb of ozone than a 65 ppb standard would, and 5,100 more kids to endure multiple exposures to 

at least 70 ppb of ozone.462

Other factors also indicate that a 65 ppb standard would be significantly more protective 

than a 70 ppb standard. The level 70 ppb would “virtually eliminate” even single exposures to 

the benchmark 80 ppb and would yield “important reductions, compared to the current standard,” 

for the benchmarks 70 and 60 ppb (about 70% for 70 ppb and about 50% for 60 ppb)—meaning 

that exposures to 70 and above would persist.463 By contrast, the level 65 ppb would eliminate 

“almost all” exposures to the benchmarks of 80 and 70 ppb, and would reduce exposures to the 

60 ppb benchmark by about 80% from the current standard.464 In just the 15 areas studied, that is 

80,000 fewer kids exposed to the 70 ppb benchmark and 784,000 fewer kids exposed to the 60 

ppb benchmark.465 Those differences are substantial: EPA offers no reasoned explanation to 

conclude otherwise.

A 65 ppb level would be significantly more effective: even in the worst case, 98% to over 

99% of kids would be protected from decrements of 15% (on average, a 54% reduction from the 

current standard), and 89-99% would be from decrements of 10% (a 37% reduction).466 As noted 

above, EPA, CASAC, and the PA all have said that a 10% decrement is adverse for people with 

asthma. The contrast between the 70 and 65 ppb levels is even more striking when comparing the 

level of protection against single instances of such decrements: the 70 ppb level would be only a 

26% reduction from the current standard for 15% decrement and a 15% reduction for 10% 

decrement;

467 the 65 ppb level would be about twice as effective, making a 50% reduction from 

the current standard for 15% decrement and a 31% reduction for 10% decrement.

468

As the tables below make clear, a standard of 70 ppb would allow from tens of thousands 

to millions of sensitive individuals to experience exposures of concern, and from hundreds of 

thousands to millions of kids to endure significant, adverse lung function decrements. EPA offers 

 

460 Id. at 75,305/3-06/1.

461 Id. at 75,306/3.

462 See id. at 75,298 tbl.4.

463 Id. at 75,306/1.

464 Id. at 75,306/3.

465 See id. at 75,297 tbl.4.

466 Id. at 75,306/3-07/1.

467 Id. at 75,306/3

468 Id. at 75,307/1.
184

no explanation for why it is lawful or rational under the Clean Air Act to allow these exposures 

and effects to persist with a 70 ppb standard. Though it is itself inadequate, a 65 ppb standard 

would be about twice as protective compared to the current standard.

TABLE 23 Mean number of people with at least one daily maximum 8-hr average O3 

Exposure at or above 60ppb while at moderate or greater exertion (includes 15 urban area 

studies)

(Data derived from EPA, HEALTH RISK AND EXPOSURE ASSESSMENT FOR OZONE FINAL REPORT,

EPA-452/R-14-004A, 5-87, TABLE 5-13 (AUGUST 2014). 

Standard 8-hr 

level

School age 

children

Asthmatic 

school-age 

children

Asthmatic adults Seniors (aged 

65-95)

65 ppb 392,000 42,000 25,000 38,000

70 ppb 1,176,000 126,000 83,000 129,000

75 ppb 2,316,000 246,000 180,000 282,000

TABLE 24 Lung Function Decrements for Alternate Ozone Standards for Children (ages 

5-18) Experiencing One or More Decrements Per Season

(Data derived from 79 Fed. Reg. at 75,279 tbl.5) 

Decreased Lung 

Function

Alternate Ozone 

Standard

Number of children 

experiencing 

decrement

Average % reduction 

from current standard

≥10% 65 ppb 1,896,000 31%

70 ppb 2,527,000 15%

≥15% 65 ppb 356,000 50%

70 ppb 562,000 26%

≥20% 65 ppb 106,000 59%

70 ppb 189,000 32%

As for other health endpoints, epidemiological studies and related risk assessments also 

support the 65 ppb level over a standard of 70 ppb. EPA contends that the single-city studies 

before it show that any level between 65 and 70 ppb “would result in improvements in public 

health, beyond the protection provided by the current standard,”469 but suggests that they provide 

no basis for distinguishing between 65 and 70 ppb.470 That analysis ignores studies like Delfino 

(1997), Burnett (1997), Burnett (1999), Koken (2003), Yang (2003), and Vedal (2003), all of 

which were cited in the Staff Paper in the last ozone NAAQS review.471 For multi-city studies, 

EPA itself notes that at least one reported adverse effects where a majority of the cities would 

have met a standard of 70 ppb but not a standard of 65 ppb, and “several” reported health effects 

even though a majority of the cities studied would have met a NAAQS set at 65 ppb.472 Setting 

 

469 Id. at 75,307/3,

470 See id.

471 See U.S. EPA (2007). Review of National Ambient Air Quality Standards for Ozone: Policy Assessment of 

Scientific and Technical Information, OAQPS Staff Paper (EPA-452/R-07-07), app.3B. (See Exhibit 13). 

472 Proposed Rule at 75,307/3-08/1.
185

the standard at 65 ppb would thus accord with the underlying city data in those studies. The risk 

assessment also predicts that 65 ppb will prevent significant numbers of adverse effects that 70 

ppb will not: For deaths tied to short-term exposure, when using 40 ppb as the cutoff for deaths 

caused by ozone, a 70 ppb standard would reduce deaths by 10%, while a 65 ppb standard would 

reduce deaths by 50% (both over the current standard); with 60 ppb as the cutoff, a 70 ppb 

standard would reduce deaths by 50-70%, and 65 ppb would reduce them by over 80%.473

EPA suggests that setting the standard at 65 ppb would require it to weigh various 

“uncertainties” less and the importance of reducing various “exposures of concern” and lung 

function decrements more.474 But EPA cannot rely on assertions of uncertainty when faced with 

scientific findings by CASAC and scientific evidence that adverse effects are likely at 65 ppb. As 

noted elsewhere in these comments, CASAC and EPA’s own staff have found, based on the 

scientific record, that adverse effects are likely at ozone levels above 60 ppb. Even if there were 

some doubt, the Clean Air Act’s “precautionary and preventative orientation” reflects that 

“Congress directed the Administrator to err on the side of caution in making the necessary 

decisions.” Lead Indus. Ass’n, 647 F.2d at 1155. 

For similar reasons, EPA could not lawfully or rationally find that a standard of 70 ppb 

would be sufficiently protective to satisfy the Administrator’s statutory obligations to set the 

standard at a level that avoids adverse effects and provide an adequate margin of safety. CASAC 

has found that “[a]t 70 ppb, there is substantial scientific certainty of a variety of adverse 

effects.”475 Indeed, CASAC repeatedly made clear that adverse effects are virtually certain at 70 

ppb: it said that the adverse combination of decrements and symptoms occur in healthy 

individuals at 72 ppb and “these effects almost certainly occur in some people, including 

asthmatics and others with low lung function who are less tolerant of such effects, at levels of 70 

ppb and below”;476 and it also said that “[a]t a level of 70 ppb for the averaging time and form of 

the current standard, clinical and epidemiological studies show adverse effects to human 

health.”

477 To establish a standard at 70 ppb, EPA would have to explain why, as a scientific 

matter, it disagrees with CASAC’s finding. Mississippi, 744 F.3d at 1357-58. As further 

discussed elsewhere in these comments, it has not done so. Thus, again, EPA has also failed to 

explain how a 70 ppb standard would be set at a level where ozone does not cause adverse 

effects. See Coal. of Battery Recyclers Ass’n, 618 F.3d at 618.

EPA has also not explained how the 70 ppb level provides an adequate margin of safety. 

As explained elsewhere in these comments, EPA has arbitrarily failed to explain what its 

approach is for accounting for the margin of safety. To the extent EPA appears to consider 

relevant factors, its purported concerns about “uncertainty” seem only to drive it toward setting a 

less protective standard.478 That is precisely the opposite of the orientation of the Act and is thus 

unlawful and irrational. E.g., Lead Indus. Ass’n, 647 F.2d at 1155 (“orientation” of the Act is 

 

473 Id. at 75,308/3.

474 See id. at 75,309/1-2.

475 CASAC Letter 2014a at 8.

476 Id. at 6; see also id. at 5 (explaining that the combination of decrements and statistically significant increase in 

respiratory symptoms is adverse)

477 Id. at 7

478 See, e.g., Proposed Rule at 75,309/2 (suggesting that a 70 ppb standard would more heavily weigh various 

uncertainties).
186

toward protection and precaution); see, e.g., NRDC v. EPA, 2014 WL 7269521, at *13 (D.C. Cir. 

Dec. 23, 2014) (where EPA action is “is ‘untethered to Congress’s approach,’” it is unlawful); 

Ass’n of Private Sector Colleges v. Duncan, 681 F.3d 427, 448 (D.C. Cir. 2012) (agency failed to 

explain elimination of “safe harbor” that was consistent with statutory “goal”).

Further, as CASAC suggested, 479 a 70 ppb level (and nearby levels) does not provide a 

margin of safety, and EPA has not explained how it does. EPA acknowledges that (1) healthy 

young adults experience adverse effects when exposed to 72 ppb ozone over 6.6 hours;

480 (2) 

CASAC found that if “subjects had been exposed to ozone using the 8-hour averaging period 

used in the standard..., adverse effects could have occurred at lower concentration”;481 and (3) 

the PA found that “significant increases in respiratory symptoms combined with lung function 

decrements” are a combination that “is likely to occur to some degree in healthy adults with 6.6-

hour exposures to concentrations below 72 ppb, and also are more likely to occur with longer 

(i.e., 8-hour exposures).”

482 Thus, even if a focus on the upper end of EPA’s proposed standard 

range were appropriate, to apply an adequate margin of safety for healthy young adults, EPA 

would have to establish a standard below 72 ppb. Nowhere does EPA explain why 2 ppb would 

be adequate both to prevent adverse effects and assure an adequate margin of safety. The lack of 

explanation is particularly problematic given that EPA mischaracterizes what the PA said. Rather 

than warning of adverse effects below “72 ppb,” as EPA intimates, the PA said that “respiratory 

symptoms combined with lung function decrements are likely to occur to some degree in healthy 

adults with 6.6-hour exposures to concentrations below 70 ppb, and are more likely to occur with 

8-hour exposures to 70 ppb and below.”483

As was the case in the 2006 PM NAAQS, see Am. Farm Bureau Fed’n, 559 F.3d at 525-

26, EPA also fails to explain how a 70 ppb (and nearby levels) standard could provide an 

adequate margin of safety for sensitive populations. Nothing in EPA’s discussion of how such a 

standard might provide an adequate margin of safety even mentions protecting sensitive 

populations.484 Yet EPA acknowledges that (1) “at-risk groups...could experience larger and/or 

more serious effects” than these healthy young adults;

485 (2) “subjects with asthma appeared to 

be more sensitive to acute effects of O3 in terms of FEV1 and inflammatory responses than

healthy non-asthmatic subjects”;486 and (3) CASAC made the scientific finding that “the level at 

which adverse effects might be observed would likely be lower for more sensitive subgroups, 

such as those with asthma.”

487 Moreover, CASAC made an even stronger scientific finding than 

EPA gives it credit for: that the adverse combination of decrements and respiratory symptoms 

“almost certainly occur in some people, including asthmatics and others with low lung function 

who are less tolerant of such effects, at levels of 70 ppb and below.”488 Thus, EPA has not 

explained how a 70 ppb level (and nearby levels) could provide an adequate margin of safety for

 

479 CASAC Letter 2014a at 8 (“a level of 70 ppb...may not meet the statutory requirement to protect public health 

with an adequate margin of safety.”)

480 E.g., Proposed Rule at 75,304/3

481 Id. at 75,305/1 (agreeing that adverse effects “could occur following exposures at least somewhat below 72 ppb”)

482 Id. at 75,296/2.

483 Policy Assessment at 4-11 (emphasis added). 

484 Proposed Rule at 75,309/1-2.

485 Id. at 75,288/3

486 Id. at 75,265/3

487 Id. at 75,287/1, 75,296/2 n.127 (quoting CASAC 6-26-14 Letter at 5)

488 CASAC Letter 2014a at 6 (emphasis added).
187

both the healthy young adults who experience adverse effects at 72 ppb and the sensitive 

subpopulations who experience adverse effects at levels below 72 ppb. Nor has EPA explained 

how a standard at 70 ppb (and nearby levels) would provide any margin of safety for sensitive 

groups, and, as further discussed elsewhere in these comments, EPA has not explained any 

departure from CASAC’s scientific conclusion that adverse effects in sensitive groups “almost 

certainly occur...at levels of 70 ppb and below.” 

Finally, we note that in the previous ozone NAAQS review (concluding in 2008), EPA 

took the position that to provide requisite protection for public health and an adequate margin of 

safety, the standard “must be set at a level appreciably below 0.080 ppm, the level at which there 

is considerable evidence of effects in healthy people.”489 EPA went on to find that “appreciably 

below” meant 0.005 ppm (5 ppb) below, and set the standard at 0.075 ppm (75 ppb). In the 

current review, EPA’s staff has found that adverse effects in healthy people are likely to occur at 

70 ppb and below (finding that the evidence supporting the occurrence of adverse respiratory 

effects is strongest for exposures at or above the 70 and 80 ppb benchmarks).490 Thus, to set the 

standard at a level “appreciably below” the level at which adverse effects are likely in healthy 

people in a manner consistent with EPA’s 2008 NAAQS decision, EPA would need to set the 

standard no higher than 65 ppb. EPA offers no reasoned basis for adopting a less protective 

approach (or less protective definition of “appreciably below”) in the current review than it did 

in 2008. 

F. Public Welfare Secondary National Ambient Air Quality Standard for Ozone

1. Introduction

Secondary National Ambient Air Quality Standards (NAAQS) must protect the public 

welfare from any known or anticipated adverse effects of air pollution. This standard is 

distinguishable from the primary human health-based NAAQS as it encompasses safeguards for 

terrestrial and aquatic ecosystems including wildlife and vegetation. In the context of ozone 

pollution, the standards must protect against any known, or anticipated adverse effects from 

ozone present in the air. In particular, plants are at increased risk. Adverse effects include 

disruption of normal storage of nutrients and carbon, direct visible damage to foliage, and 

climate change. These impacts directly translate to public welfare harm due to the effects on crop 

and forest productivity, resilience, scenic beauty, ecosystem functioning, and climate change. 

The EPA is charged with reviewing the latest science and evaluating the protectiveness of 

both the primary and secondary standards every five years under the Clean Air Act NAAQS 

process. To date the secondary standard for ozone has been set at the same level and form as the 

primary health standard, even in the face of the past three reviews that provided significant 

science-based evidence that this was not protective of the public welfare. 

 

489 73 Fed. Reg. at 16,480 (Mar. 27, 2008); see also id. at 16,483 (standard should be set at level that “is appreciably 

below 0.080 ppm, the level in controlled human exposure studies at which adverse effects have been 

demonstrated”).

490 Policy Assessment at 4-11; see also Proposed Rule at 75,305/2 (finding that the evidence supporting the 

occurrence of adverse respiratory effects is strongest for exposures at or above the 70 and 80 ppb benchmarks).
188

Our organizations believe that EPA must set a W126 standard of 7 ppm-hrs to be 

protective of tree growth, foliar health, and to mitigate anthropogenic climate change. This form 

and level reflects the best protection promoted by the CASAC and by the National Park 

Service.

491 We are dismayed that EPA has left the secondary standard in the shadows in its 2014 

proposal. Of particular concern is EPA’s unwillingness to propose a W126 standard despite the 

Agency’s clear recognition that this is the correct metric to characterize impacts to vegetation. 

Such an approach is unlawful and arbitrary. Further, in selecting the form of the standard and 

level of protection, the Agency has arbitrarily rejected or ignored advice input from CASAC and 

the National Park Service. EPA appears to have selected a range of 13-17 ppm-hrs based on the 

Agency’s estimated equivalency with the primary range of 65-70 ppb rather than as a matter of 

public welfare protection. EPA has failed to rationally justify advancing this deficient standard 

for public welfare and as such it must be corrected to reflect the recommendation of its scientific 

advisors and federal land managers.

The EPA Administrator is taking comment on the W126 as the alternative form of the 

secondary NAAQS, as well as a level as low as 7 ppm-hrs as recommended by CASAC and 

which we support. We urge Administrator McCarthy to set the standard using the W126 form 

which has been clearly demonstrated as the most scientifically relevant form to protect 

vegetation. The standard must reflect the fact that ecosystems and species respond differently to 

ozone pollution than humans. Protection of the above-described welfare values is at the core of 

this decision. 

In consideration of the advice of CASAC, the position of the National Park Service, and 

the clear science that demonstrates impacts on tree growth and foliar damage at levels greater 

than 7 ppm-hrs, we urge the Administrator to select this level of protection. Finally, 

consideration of the conservative approach of calculating the W126, which limits the summation 

window to only 12 daylight hours, only 3 months of the growing season, and the averaging 

across a 3 year window, further supports selection of the level of 7 ppm-hrs because it would 

afford the level of protection requisite to protect public welfare. 

2. Secondary NAAQS must protect public welfare 

Section 109(b)(2) of the Clean Air Act states that the secondary standard must “specify a 

level of air quality the attainment and maintenance of which, in the judgment of the 

Administrator, based on such criteria, is requisite to protect the public welfare from any known 

or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.” 

EPA must base its decision on the significant body of science brought forth in the 

Integrated Science Assessment (ISA), the Welfare Risk and Exposure Assessment (WREA), as 

well as the advice of CASAC and the National Park Service. These authorities all strongly 

support a separate secondary standard, and one far more protective than EPA has proposed. 

In selecting a form to protect vegetation EPA must use the best biologically relevant 

metric. The W126 metric has been recommended to EPA (and found by the EPA Administrator 

 

491 NPS Letter N3615 (2350) Mar. 20, 2014.
189

herself) as being the most biologically relevant form in this current review, as well as in the 2006 

review and the 2010 reconsideration. 

a. Adverse effects to vegetation and ecosystems

Adverse effects from ozone include disruption of normal storage of nutrients and carbon 

and direct visible damage to foliage. These impacts directly translate to public welfare harm due 

to the effects on crop and forest productivity, resilience, scenic beauty, and ecosystem 

functioning. In terms of ecosystem services impacts include, but are not limited to, cultural (e.g. 

recreation) and product (e.g. agriculture) related services. 

In this review EPA is clear that ozone exposures on vegetation and ecosystems are widespread and pervasive. The final 2013 ozone ISA documents the ecosystem effects that the 

Agency considers causal and likely casual, including:492 

o Visible injury to plants and tree foliage effects

o Reduced vegetation growth

o Reduced productivity in terrestrial ecosystems

o Reduced yield and quality of agricultural crops

o Alteration of below ground biogeochemical cycles 

o Alteration of terrestrial ecosystem water cycling

o Reduced carbon sequestration in terrestrial ecosystems

o Alteration of terrestrial community composition

As outlined in the most recent review the latest science has advanced our understanding 

around ozone’s role in disrupting below ground processes including carbon storage. This has 

important ramifications related to carbon sequestration and mitigation of greenhouse gas 

emissions. 

The causal effects defined above clearly show that when ozone is present in the ambient 

air there are significant and multiple costs to vegetation, and while some species are more 

sensitive than others it is also recognized that there is a cumulative impact for the ecosystem, 

wildlife habitat, and larger landscapes. This ubiquitous effect of ozone pollution must be 

addressed in setting the public welfare standard.

 

b. Adverse effects to climate

Our groups are concerned that the proposed rule does not properly characterize the 

welfare impacts of radiative forcing from ozone. Ozone not only harms vegetation, but also is a 

potent greenhouse gas. The ISA states that there is a “relationship between the changes in 

tropospheric O3 concentrations and effects on climate.”

493 The proposed rule also states that “the 

evidence supports a causal relationship between changes in tropospheric O3 concentrations and 

radiative forcing.”494 While it is true, as outlined in the ISA, that there are a number of details 

related to ozone’s climate impacts that have not been resolved, the important facts are known. 

 

492 ISA, Table 1–2.

493 See ISA at 2–47. 

494 Proposed Rule at 75234, 75315. 
190

First, it is clear that ozone has a strong warming impact, especially in Northern mid-latitudes 

(where the United States is) and in the Arctic. Second, whatever its exact radiative forcing, ozone 

is the third strongest greenhouse gas. Third, it is well-established that ozone can be reduced 

through decreases in methane, carbon monoxide and VOCs. As EPA acknowledges, reducing 

these precursors would significantly benefit public health as well as climate. Consequently, we 

urge Administrator McCarthy to consider the direct as well as indirect climate impacts of ozone 

as she makes her judgment about setting the level of the secondary standard. 

i. Direct Climate Impacts in the Arctic

The Arctic region deserves special consideration both due to the Class I areas located 

within Alaska495 near the Arctic Circle and because ozone-mediated climate impacts in the 

Arctic have implications for the contiguous United States. 

Ozone has a larger impact in the Arctic than in other regions.496 This is so both because 

ozone remains in the atmosphere longer than average in the Arctic Winter and Spring497 and 

because ozone is most effective at absorbing shortwave radiation, such as that reflected from 

snow and ice, in the Arctic.498 In fact, ozone is estimated to exert a radiative forcing of 

approximately 1 W/m2during the Arctic summer499 and to have increased temperatures as much 

as 0.5 °C in the winter and spring in the Arctic in the last century.500

The Arctic is a unique region that hosts an intricate and highly specialized ecosystem. 

Many of the species in the region are the last survivors from the previous ice age. Because the 

environment is harsh, species in the Arctic are highly adapted to survive in a narrow range of 

conditions. Furthermore, the inhabitants of the Arctic have no options for migration in the face of 

a warming environment: they are already as far north as possible and there is no higher elevation 

to which these species can climb. Arctic species rely upon fundamental features of the Arctic 

landscape, such as sea ice, permafrost, and seasonal snowpack. Yet, these features are currently 

teetering on the brink of various climatic “tipping points.” 

The Arctic is currently experiencing climate changes of a magnitude not experienced 

anywhere else on Earth. For instance, the Arctic is warming at twice the rate of the rest of the 

world.501 Furthermore, sea ice is melting at precipitous and unprecedented rates.502 Greenland ice 

sheets are contracting at accelerating rates and permafrost is experiencing deeper and more 

frequent freeze/thaw cycles. 

 

495 The Class I areas within Alaska are: Denali National Park, Bering Sea Wilderness Area, Simeonof Wilderness 

Area, and Tuxedni Wilderness Area. 40 CFR Part 81, Subpart D.

496 ISA sec. 10-13,14,18.

497 ISA at 10-18.

498 ISA at 10-13.

499 ISA at 10-13.

500 ISA at 10-18.

501 IPCC (2007). CLIMATE CHANGE 2007: SYNTHESIS REPORT at 30.

502 See, e.g., J. Stroeve et al. (2008). Arctic Sea Ice Extent Plummets in 2007. Eos, Transactions, American 

Geophysical Union 89(2): 13-14; R. Kwok & D.A. Rothrock, Decline in Arctic sea ice thickness from submarine 

and ICESat records: 1958-2008, Geophys. Research Letters, 36, 15501.
191

Adverse impacts resulting from the accelerated loss of Arctic sea ice extend well beyond 

the Arctic Ocean and its coast. By reflecting the sun’s energy back into space, sea ice is an 

effective insulator, preventing heat in the Arctic Ocean from escaping upward and warming the 

lower atmosphere.503 The decline of sea ice amplifies warming in the Arctic, which in turn has 

major implications for temperature patterns over adjacent, permafrost-dominated land areas and 

for weather patterns across the Northern Hemisphere.504 Higher temperatures will thaw out 

extensive expanses of permafrost, resulting in the potential release of methane and carbon 

dioxide currently frozen in Arctic soils, thereby accelerating further warming.505 Additional 

warming in the Arctic resulting from the loss of sea ice will also affect weather patterns by 

altering atmospheric circulation patterns, leading to more extreme weather events and affecting 

transportation, agriculture, forestry and water supplies.506 Loss of sea ice in the Arctic Ocean will 

therefore have serious repercussions as climactic feedbacks resulting from higher temperature 

increases accelerate, the timing of the seasons is altered, and shifting circulation patterns cascade 

through the Arctic and beyond. 

These climate impacts will directly affect proximate Class I areas within Alaska. In 

addition, a strong secondary standard for ozone is a critical part of the overall effort to avoid 

cascading catastrophic consequences for the lower 48 states. 

c. Ecosystem Services 

In this review EPA clearly delineates Ecosystem Services as a construct to assess the 

relationships between ozone impacts to vegetation and resultant impacts on public welfare. 

Ozone pollution has both direct ecological impacts on ecosystem services, such as the damage 

that happens to plant and tree foliage when exposed to ozone, as well as the resulting impacts to 

cultural (e.g., recreation) and product (e.g., agriculture) related services. Ecosystem Services 

establish the benefits received from specific species or ecosystems. In characterizing the impact 

to public welfare in this way, EPA has access to a construct through which the agency may 

develop methods to assess what might be expected to change under air quality scenarios 

representing varying alternatives for a secondary standard. We strongly agree with EPA’s 

recognition that some benefits cannot be marketed and are difficult to quantify but are highly 

valued in the context of the public welfare nonetheless. 

d. Protecting Public Lands

We agree with EPA Class I areas (National Parks, Wildernesses, Forests, and Refuges) 

hold special value and context to the public and therefore warrant strong protection. Air 

pollution that harms ecosystems and scenic beauty in these national public lands adversely 

affects public welfare because, among other things, these special places were set aside for 

conservation of their natural values, for use and enjoyment by the public, and under the Clean 

 

503 World Wildlife Fund Int’l (2009). ARCTIC CLIMATE FEEDBACKS: GLOBAL IMPLICATIONS at 8 (M. Sommerkorn & 

S. Hassol eds.) at 19-20.

504 Id. at 18.

505 Id.

506 J. Francis & S. Vavrus (2012). Evidence Linking Arctic Amplification to Extreme Weather in Mid Latitudes, 39 

Geophys. Research Letters, L06801.
192

Air Act, as places to have the most pristine air quality. 42 U.S.C. 7472. EPA must limit the

impacts from ozone pollution to Class I areas to fulfill, and act consistently with, the 

Congressional mandates to protect and preserve these places for the foregoing purposes. 

Advancing protections to safeguard the air and resources in these areas is critical to the meeting 

the Clean Air Act objective. 

In giving priority to these areas, the Administrator must consider that Class I areas 

include many mountain systems that can have high background ozone with little change in 

diurnal concentrations, even during the daylight hours. Consequently, when ozone pollution 

events occur they build upon these high background levels and therefore exacerbate overall 

cumulative impacts. Class I areas also include many wetland ecosystems, that support 

significant diverse wildlife, and where foliar injury from ozone can be more severe. 

In addition to the ozone impacts to vegetation, EPA must consider the climate change 

impacts of ozone in Class I areas. Ozone increases radiative forcing, which in turn exacerbates 

climate harms in national parks and other Class I areas. National parks are significantly 

threatened by a rapidly warming planet. Impacts range in degree and breadth and include coastal 

areas affected by rising oceans, deserts experiencing extreme heat events, and alpine regions 

beleaguered by extended drought. 

For example, rising sea levels in Florida’s Everglades National Park threaten the 

mangrove ecosystem that filters saltwater and thereby preserves freshwater wetlands. Rising 

temperatures and drought in New Mexico’s Bandelier National Monument have driven bark 

beetles to higher elevations, causing high mortality rates to the piñon pines. Rising temperatures 

in Yellowstone National Park are also killing whitebark pine trees, which translates to reduced

chances of grizzly bear survival in Yellowstone because grizzlies rely heavily on whitebark pine 

seeds as a critical source of nutrition. Warmer temperatures in Great Smoky Mountains National 

Park could increase ozone levels, further damaging critical tree and plant species. Scientists 

have linked these and other changes occurring in our national parks directly to climate change.

In 2014, NPS published a study that examined the extent to which 289 parks are 

experiencing extreme climate changes when compared to the historical records from 1901–

2012.

507 Results show that parks are overwhelmingly at the extreme warm end of historical 

temperatures. The 2014 Parks Study also points to changes in precipitation patterns since 1901. 

These findings are supported by previous scientific research. Parks that have been experiencing 

extremely warm and dry climates include Kalaupapa National Historical Park in Hawaii, Mojave 

National Preserve in southern California, and Lake Mead National Recreation Area in Nevada 

and Arizona. Parks that have become extremely warm and wet include Cape Lookout National 

Seashore in North Carolina, Florissant Fossil Beds National Monument in Colorado, and 

Delaware Water Gap National Recreation Area in New Jersey and Pennsylvania. 

The Appalachian National Scenic Trail (ANST) was designated as a unit of the National 

Park System and the first National Scenic Trail in 1968. The Appalachian Trail follows the hills 

and valleys of the Appalachian mountain range in the eastern United States. The 2014 Parks 

 

507 Monahan & Fisichelli (2014) Climate Exposure of US National Parks in a New Era of Change. [hereafter 2014 

Parks Study]
193

Study found the recent mean temperatures on the ANST were ranked as “extreme warm” 

compared to the historical data set. Further, climate data collected at a northern ANST midelevation site in the White Mountain National Forest, where winter recreation is very important 

to local economies, show that snowpack is disappearing 15 days earlier in the spring and annual 

snowfall has declined by 69 inches over the time period of 1935-2012.

508

According to the 2014 Parks Study, species within national parks are experiencing 

extreme climates, causing changes to plant and animal behavior. For example, temperate tree 

species in the Great Lakes region appear most sensitive to higher summer temperatures, while 

white-tailed deer are more sensitive to winter conditions. 

Taken together, these data show that welfare effects from climate change—including at 

least some contributing effect from tropospheric ozone—not only can be “anticipated,” but in 

fact are already occurring in the nation’s National Parks and other Class I areas. EPA must 

address the dire need to reduce direct climate impacts from ozone, in addition to addressing 

vegetation effects, when setting the standard.

All publicly protected lands are visited for recreation and rejuvenation and are often 

important wildlife habitat areas. This nexus of sensitive ecological systems with the significant 

ecosystem services must be weighted in the context of the public welfare. 

3. Scientific Consensus Supports a Different Form 

a. Support for a Cumulative Seasonal W126 Standard 

The scientific foundation supporting the use of a cumulative standard to protect 

vegetation began in the 1996 review. At that time EPA had a significant amount of science 

recognizing that the form of the standard used to protect human health was not appropriate for 

protecting vegetation. In the 2006 review, again in the reconsideration in 2010, and in the 

current review EPA clearly supports the main assertions that ozone’s impact on vegetation is 

cumulative and that higher ozone concentrations are more important in causing measureable 

impacts to plants than lower concentrations. This is the foundation for the W126 metric which 

sums the seasonal ozone exposure and uses a sigmoidal weighting function to weight higher 

concentrations more than lower levels. EPA has continued to focus on this type of metric as the 

“most biologically relevant metrics for consideration of O3 exposures eliciting vegetation-related 

effects. Such a metric has an ‘‘explanatory power’’ that is improved ‘‘over using indices based 

on mean and peak exposure values.’’509 As shown in the record for the current rulemaking, 

CASAC and EPA’s staff have repeatedly and unequivocally recommended adoption of this 

metric for the secondary ozone standard.

Considering this long standing support of the W126 metric, vetted in two reviews (and 

one re-consideration) over a nearly 20 year period it is clear that the implementation of this 

metric is too long delayed. EPA must adopt this metric as the standard instead of the health 

based metric that is used for the primary health standard. 

 

508 AMC unpublished data.

509 ISA sec. 2.6.6.1, at 2–44.
194

b. 8-hr Form Is Not Protective of the Public Welfare 

EPA cannot lawfully or rationally set a national welfare standard based on a metric 

designed to protect public health. It is arbitrary and unlawful for EPA to propose a welfare 

standard in the 8-hour form in direct contradiction with its own conclusion that public welfare 

protection is – as a matter of science - appropriately judged through the use of the cumulative 

seasonal W126-based metric. EPA has again disregarded CASAC’s advice that is founded on a 

plethora of scientific information and context built in this review and past reviews. This is the 

very definition of an arbitrary and capricious decision.

Moreover, EPA fails to offer a full scientific (or indeed any) basis for rejecting CASAC’s 

advice on this issue, as the law requires. See part V.C. above. The agency makes no claim that 

reliance on the 8-hour form will do a better job of protecting welfare than the W126 form, and 

indeed the record provides no support for such a claim. Nor is there any claim by the agency that 

some statutorily relevant purpose is served by foregoing the W126 metric – which the agency 

agrees is more biologically relevant and appropriate. And even if implementation concerns were 

relevant at the standard-setting stage (and they are not), EPA cites no potential implementation 

problems as a justification for foregoing the W126 metric 

Further, EPA is simply wrong in suggesting that the 8-hour primary form (3-year average 

of the 4th highest daily 8-hour average) for the ozone secondary welfare standard can adequately 

substitute for the W126 standard to protect vegetation based on alleged relationships between 

three year averaged 8-hour values and three year averaged W126 values. CASAC expressly 

rejected reliance on such comparisons, and EPA fails to fully or rationally explain why CASAC 

was error on this point. As CASAC stated:

However, as noted in the CASAC’s review of the Second Draft WREA (EPACASAC-14-003), the CASAC finds that a W126 level of 15 ppm-hrs may not be 

similar to the current standard, since the actual approaches that would be used to 

achieve such a level are likely to be different than those assumed in the HREA air 

quality scenarios for just meeting the current standard. Specifically, and quoting 

from our review of the Second Draft WREA: 

“The currently reported finding of only small differences in risk between just 

meeting the current standard and a W126-based level of 15 ppm-hrs must not be 

interpreted to mean that just meeting the current standard will be as protective as 

meeting a W126-based standard at 15 ppm-hrs. There are two key factors that 

must be considered when making this comparison. First, air quality was simulated 

in the Second Draft WREA based on the magnitude of across-the-board 

reductions in NOx emissions required to bring the highest monitor down to the 

target level. Meeting a target level at the highest monitor requires substantial 

reductions below the targeted level through the rest of the region. This artificial 

simulation does not represent an actual control strategy and may conflate 

differences in control strategies required to meet different standards and different 

targets. As a result, there may be a number of monitors that meet the current 
195

standard but would not meet an alternative W126 standard. Second, and equally 

important, the current form of the standard is much less biologically relevant for 

protecting vegetation than is a seasonal, peak weighted index such as the W126, 

which was designed to measure the cumulative effects of ozone exposure.” 510

EPA offers no rational response to the above CASAC rationale. 

The Policy Assessment likewise found that there was no consistent relationship between 

8-hour and W126 levels:

[W]hile the western sites that are influenced by upwind urban plumes may have 

increased cumulative seasonal values coincident with increased daily 8-hourpeak 

O3 concentrations, this analysis indicates that, in sites without such an urban 

influence (the eastern sites in this analysis), such a relationship does not occur 

(U.S. EPA, 2013a, section 3.6.3.2). Thus, the lack of such a relationship indicates 

that in some locations, O3 air quality patterns can lead to elevated cumulative, 

seasonal O3 exposures without the occurrence of elevated daily maximum 8-hour 

average O3 concentrations (U.S. EPA, 2013a, section 3.6.3.2). Further, staff notes 

that the prevalence and geographic extent of such locations is unclear, since as in 

the last review, there continue to be relatively fewer monitors in the western U.S., 

including in high elevation remote sites. . . . . ...O3 concentrations measured in 

some rural sites can be higher than those measured in nearby urban areas (U.S. 

EPA, 2013a,section 3.6.2.2) and the ISA concludes that ‘‘cumulative exposures 

for humans and vegetation in rural areas can be substantial, and often higher than 

cumulative exposures in urban areas’’(U.S. EPA, 2013a, p. 3–120). These known 

differences between urban and rural sites suggest that there is the potential for an 

inconsistent relationship between 8-hour daily peakO3 concentrations and 

cumulative, seasonal exposures in those areas.

Proposed Rule at 75,344 (emphasis added).

EPA cites511 an analysis in the PA of design values at monitors for 2001-03 and 2009-11 

that purportedly shows that between the two periods during which broad scale precursor 

reductions occurred, ozone reductions in terms of both metrics were recorded, and there was a 

fairly strong positive degree of correlation between the two metrics. In support, the notice says:

 in 2009-11, monitors just meeting the current standard (75ppb) had W126 values 

ranging from less than 3 ppm-hrs to approximately 20 ppm-hrs

 At sites with an 8-hour design value at or below 70 ppb, 3-year W126 values were 

above 17 ppm-hrs at no monitors, above 15 ppm-hrs at 1 monitor, and above 13-ppmhrs at 8 monitors in the West and Southwest

 At sites with 8 hour design value at or below 65 ppb, W126 values were above 11 

ppm-hrs at no monitors, above 9 ppm-hrs at 3, and above 7 at 9 (majority of which 

are located in the West and Southwest)

 

510 CASAC Letter 2014a at 11 (emphasis added). 

511 Proposed Rule at 75,344-45.
196

These data do not support a claim of congruence between the primary standards being 

considered and the W126 options. First, the data show that there were in fact a number of 

monitors that would meet the various 8-hour standard levels yet violate W126 levels that are 

within the CASAC and PA ranges. Second, even as to sites where both standards would be met, 

there is no basis for concluding that there is some fundamental underlying relationship that 

assures meeting the 8-hour will mean meeting any of the W126 options: indeed the above quotes 

from the PA and CASAC refute such a suggestion. Finally, the periods examined include the 

recession of 2008-10: hardly a representative period, as industrial activity and emissions 

declined.

EPA also cites another analysis in PA that looks at data for 3-year periods back to 2006-

08 and indicates that among counties that met the current standard, the number with W126 

values above 15 ppm-hrs ranges from fewer than 10 to 24 (these were predominantly in the 

Southwest region. Again, the analysis fails to show that meeting an 8-hour standard will 

invariably – or even very likely – meet a W126 standard. It addresses only a comparison with 

the current (inadequate) 75 ppb standard, it looks only at counties that would have been over 15 

ppm-hrs, and it still finds that a number of counties would violate a W126 standard: And it 

suffers from the same defects cited above.

Additional analysis shows that an 8-hour standard metric would in fact allow a wide 

spread variation in W126 values. This variability increases as the level of the standard moves 

away from 60 ppb to higher 8-hour averages. Further, this approach is particularly underprotective in western National Parks and other Class I areas in this region, where the relationship 

between EPA’s target W126 values and the 8-hour metric is least robust (as reported by Wells). 

EPA relies in large part on an analysis512 that compares the W126 to 8-hour513 form 

levels to assert that EPA can achieve a level of protection defined by the W126 metric but 

represented by the 8-hour form. This approach is flawed in both general application and when 

specific western US National Parks are examined. 

Figure 13. Wells (2014) 

nationwide data comparing 3 

year averaged W126 to 8-hr 

values from 2001-2013. 

Expanded view shows range 

of W126 values at 60, 65, and 

70 ppb.

 

512 B. Wells (2014). Comparison of Ozone Metrics Considered in the Current NAAQS Review, U.S. EPA, available 

at http://www.epa.gov/ttn/naaqs/standards/ozone/data/Wells-2014-CompO3Metrics-EPA-HQ-OAR-2008-0699-

0155.pdf .

513 The primary 8-hour average calculations incorporate the 2014 proposed change to limit to only 17 8-hour 

averages of each day
197

The relationship is clearly non-linear with significant spread in the data, see Figure 13. 

Table 25 shows the minimum, maximum, and range in W126 values observed at levels of 60, 65, 

and 70 ppb from a dataset used in the Wells memo.

514

 Particularly noteworthy is the large 

variation of W126 values for each 8-hour level, with range of 4.9, 8.9 and 15.3. This level of 

variability shows that the 8-hour metric is simply not an accurate surrogate for W126 levels. And 

the decree of variability is material and substantial. For example, at the 8-hour level of 70 ppb, 

some sites have 3 year average W126 values higher than CASAC high end of 15 ppm-hrs and 

EPA’s proposed high end of 17 ppm-hrs. Although the variability is less at an 8-hour level of 65 

ppb, the range of W126 levels is a full 8.6 ppm-hrs: equivalent to more than 50% of the high 

ends of both the CASAC and EPA ranges. And the maximum W126 level at 65 ppb is 11.8 

ppm-hrs, far in excess of the 7 ppm-hrs low end of the CASAC and staff ranges. The variability 

in these ranges is all the more significant considering the conservative approach to calculating 

the W126, e.g. 3 year average, limited to 12 hr and highest 3 months. For all these reasons, it is 

arbitrary for EPA to suggest that the Wells data shows that 8-hour form will achieve target W126 

based levels of protection. 

Table 25. Significant variability in three year average W126 ranges at three year average 8-hour 

level targets from Wells Memo dataset. 

8-hour level 

(ppb)*

Minimum 

W126

Maximum 

W126

Range in 

W126

60 2.0 6.9 4.9

65 3.2 11.8 8.6

70 3.8 19.1 15.3

*Levels based on ppm values truncated to 3rd decimal place

Wells identified that the relationships between the metrics vary by region stating: “In 

particular, the Southwest and West regions (i.e., the southwestern U.S.) appear to have higher 

W126 values relative to their respective 4th max values than the rest of the U.S.”515 Here, we 

provide some specific analysis of 11 western National Parks included in the Wells dataset that 

further exemplify the inter-site variability, uncertainties in predicting W126 values, and underprotection of western park lands using the 8-hour standard. We applied linear regressions 

between the W126 and 8-hour metrics for individual park level data and found significant 

variability is present when moving from one location to another even among the western region 

sites. 

The parks included were: Chiricahua National Monument, Grand Canyon National Park, 

Petrified Forest National Park, Death Valley National Park, Joshua Tree National Park, Lassen 

Volcanic National Park, Mesa Verde National Park, Big Bend National Park, Chamizal National 

Memorial, Canyonlands National Park, and Great Basin National Park. All of these parks have 

ozone-sensitive species (see Exhibit 14). At the 60 ppb level two parks exceeded a level of 7 

ppm-hrs; Chiricahua National Monument and Joshua Tree NP had W126 values of 9.6 and 10.1 

ppm-hrs, respectively. At the levels EPA proposed, 65 to 70, all of the 11 parks exceed 7 ppm-

 

514 Provided by B. Wells via email.

515 B. Wells (2014). Comparison of Ozone Metrics Considered in the Current NAAQS Review, U.S. EPA, available 

at http://www.epa.gov/ttn/naaqs/standards/ozone/data/Wells-2014-CompO3Metrics-EPA-HQ-OAR-2008-0699-

0155.pdf.
198

hrs and 6 out of 11 exceed 15 ppm-hrs, the high end of the range recommended by CASAC, and 

1 park (Joshua Tree NP) exceeded the 17 ppm-hrs at an 8-hour standard of 70. 

Table 26. The range in W126 values associated with 8-hour targets, calculated from linear fits 

for 11 National Parks included in the Wells dataset. 

8-hour 

level (ppb)

Minimum 

W126

Maximum 

W126

Range in 

W126

# of parks > 

W126 level

60 2.5 10.1 7.4 2 parks > 7

65 3.2 11.8 8.6 11 parks > 7

5 parks > 10

70 3.8 19.1 15.3 6 parks >15

CASAC clearly emphasized its opposition to averaging the W126 standard over 3 years 

pointing to the cumulative nature of ozone impacts and the fact that a 3-year average standard 

does not protect against damage from high levels in a single year. They recommend EPA focus 

on the lower end of the 7-15 ppm-hrs range if averaging across 3 years. EPA not only ignores 

this advice but proposed averaging with an even higher W126 range target. 

We examined the annual W126 values at 4 western National Parks compared to EPA’s 

preferred 3-year averaged 8-hour maximum form for the timeframe 2000-2013. These parks 

were selected because their 8-hour values have been within and just over the range of 60-70 ppb. 

Those parks include: Grand Canyon National Park, Mesa Verde National Park, Big Bend 

National Park, and Canyonlands National Park. All 4 parks have ozone-sensitive species present 

including Ponderosa Pine an important forest tree species for western forests that have both 

commercial and ecological value516. EPA states that 15 ppm-hrs creates 3 percent loss for 

ponderosa pine.517

It is no surprise that the variability in 1 year W126 data is greater than a metric that is 

averaged over 3 years. Our concern is that this year-to-year variation in W126 is significant in 

these parks but unaccounted for in EPA’s approach. The ranges observed in W126 values on an 

annual basis would result in significant biomass loss of 6% or greater, see Table 27. In light of 

the clear recognition that ozone damage is cumulative these findings indicate that EPA’s 3 year 

averaging approach dilutes the effectiveness of setting a protective level. Further, the ranges 

observed in W126 include levels that represent a median biomass loss of 6% or greater, 3 times 

as high as CASAC threshold of less than or equal to 2%. 

Table 27. Range in annual W126 values at 4 National Parks showing significant under 

protection 

National 

Park

Standard 

Deviation 

Annual W126

Standard 

Deviation 

3 year 8-hour

Range 

Annual 

W126

Range

3 year 8-

hour

# Ozone 

Sensitive 

Species

Big Bend 3.7 3.3 4.4 - 18.0 62 - 71 4

Grand Canyon 4.3 2.2 10.1 - 26.9 68 - 74 12

 

516 Greater Flagstaff Forests Partnership, Ecology of Southwestern Ponderosa Pine Forests, available at 

http://www.gffp.org/pine/ecology.htm. 

517 Proposed Rule at 75,324.
199

Mesa Verde 3.9 2.0 10.7 - 23.4 67 - 73 7

Canyonlands 4.1 1.3 10.3 - 23.6 68 - 72 11

Grand Canyon, Mesa Verde and Canyonlands National Parks all had minimum values 

greater than 9 ppm-hrs, the upper end of the range cited by the National Park Service (Table 27). 

Further, these sites often see W126 levels greater than 15 ppm-hrs, the upper end of the range 

identified by CASAC, and 17 ppm-hrs (See Exhibit 14). Unfortunately, Big Bend National Park 

is seeing an overall rise in ozone reflected in both metrics. The peak W126 value of 18.0 at Big 

Bend was in 2011 while the peak 8-hr value was in 2013. In addition, 10 out of 14 years 

exceeded a level of 7 ppm-hrs at Big Bend, while only 6 of these years exceeded a 3 year 8-hour 

average of the 4th highest daily of 65 ppb. These disconnects are further examples of how the 8-

hour standard is ill-suited to protect vegetation. The 8-hour standard does not ensure secondary 

standards are protective of the values Congress intended they protect. 

4. The W126 is the right metric

a. What is the W126 and why is it more relevant to protecting 

vegetation? 

A W126 standard is different from the form upon which the primary standard is built in a 

number of key ways. This is important to articulate because it explains why the primary metric 

of the 3 year average of the 4th highest daily 8-hour average is not scientifically defensible as a 

way to protect vegetation. 

The W126 is a weighted value. The actual hourly ozone 

concentration, in ppm, is assigned a weighted value with higher 

concentrations counting more than the lowest values. This is 

based on many scientific studies that found this form best 

relates to plant damage that can be documented and measured. In 

this case the weighting formula is sigmoidal. A sigmoidal 

weighting metric is clearly different from the primary form 

where only the top 4 maximum values over a season determine 

the standard: here all values included in the summing window greater than 60 ppb are weighted 

more heavily. The W126 not only accounts for maximum concentrations but also factors in 

exceptionally high concentrations (e.g. >100 ppb) as it assigns these values the most weight.

It’s cumulative (summed). This is appropriate for looking at impacts to vegetation over 

the growing season because damage can be attributed to the ongoing exposure to the pollutant as 

the plant moves through its annual growth cycle. Clearly this is different from the primary 

standard which is based on one peak value (the 4th highest daily 8-hour maximum) and provides 

little reflection of the growing season, potentially compounding the full effects of ozone 

exposure. 

As we will discuss below it should be recognized that EPA’s summation window for 

W126 (highest 3 month 12-hr sum) is conservative and not protective of full season exposures 

(the growing season is longer than 3 months) or all environments (mountains with high ozone 
200

overnight and in the early morning). This limitation may leave some plants at higher elevations 

unprotected during overnight and early morning when ozone can be peak. Further, EPA favors a 

3 year averaging of the cumulative exposure that is counter to the CASAC recommendation to 

use a 1 year metric.

b. The CASAC recommendations 

The CASAC clearly concludes that the current secondary standard is not sufficient to 

protect vegetation from welfare effects of ozone.

518 They recommend changing the form to the 

W126 at the level of 7 to 15 ppm-hrs. Id. The CASAC “does not recommend the use of the 

three-year averaging period,” finding that use of such an averaging period “is not supported by 

the available data.”519 They instead advise a single year standard pointing out that this is more 

biologically relevant, provides more protection to annual crops, protects perennials from the 

cumulative effects of ozone exposure, and protects against single unusually damaging years.520 

They also state that if the 3-year averaging period is used that the upper limit of 15 ppm-hrs 

should be reduced.

EPA fails to provide a scientific or reasoned basis for rejecting CASAC’s 

recommendation of a single-year W126 standard. EPA cites variability in ambient ozone 

concentrations from year to year, but fails to explain why that justifies a 3-year average over a 

single year standard. As CASAC noted, the variability in a single year W126 standard is reduced 

by the fact that it is the sum of 3 months of data, so it is not nearly as sensitive to extreme events 

as an hourly or 8-hour averaging period.521 Even if there is significant variability, EPA fails to 

explain why that is relevant to assuring requisite welfare protection, and if so why the 3-year 

average approach would be more effective at protecting public welfare. EPA further asserts that 

the PA found greater significance for effects associated with multiple-year exposures, but that 

PA observation was referring to potential carry over effects from one year to the next. It does 

not show that a single year metric would provide inadequate protection, or that a 3-year average 

would provide better protection. In fact, the PA finds that use of 3-year averages may lead to 

underestimation of RBL.522 EPA further asserts that CASAC’s concern about protecting against 

adverse effects associated with a single year’s exposure “can be addressed through use of a 

three-year average metric, chosen with consideration of the relevant factors.”523 But EPA does 

not explain how such an approach can address CASAC’s concern, nor does EPA commit to 

adopting such an approach. EPA also asserts that the Administrator recognizes greater 

confidence in judgments related to public welfare impacts based on a three-year average metric, 

but fails to explain why this is so, and fails to cite scientific evidence in support. Finally, EPA 

disregards CASAC’s advice that if a 3-year average is used, it should be set at a lower level than 

a single-year standard to protect against single unusually damaging years that will be obscured in 

the average.524 EPA offers no explanation for failing to follow CASAC’s advice on this score. 

Not only does EPA fail to commit to setting such a lower level, but it proposes a range with a 

 

518 E.g., CASAC Letter 2014a at iii.

519 Id. 13. 

520 Id.

521 Id. at 13. 

522 Proposed Rule at 75338/3. 

523 Id. 75347/2. 

524 CASAC Letter 2014a at 13. 
201

high end (17 ppm-hrs) that is actually higher than the range recommended by CASAC for a 1-

year W126 standard.

For all the foregoing reasons, EPA’s rejection of CASAC’s advice for adoption of a 

single-year W126 metric is arbitrary and violative of EPA’s duty to adequately justify a 

departure from CASAC’s recommendation. 

Of note, CASAC advised that levels above 15 ppm-hrs should not be options for the 

secondary standard. By way of example, CASAC noted that at 17 ppm-hrs, the median tree 

species has an “unacceptably high” loss of tree biomass (6%). Further, they state that a level of 

“7 ppm-hrs is protective of ecosystem services” as it is the only level in which the median loss 

for the tree species examined is less than or equal to 2%.

c. A 12-hr, maximum 3 month W126 form of the standard is 

conservative 

In selecting the level of the W126 to protect public welfare, the EPA Administrator must 

consider that a form set as a 12 hour/highest 3 month sum, provides only a conservative level of 

protection due to under estimating true exposure to vegetation. First limiting to only a 3 month 

summing window is clearly not representative of the full growing season and overlapping 

elevated ozone concentrations and therefore is only a partial account of the ozone exposure. 

Second, as we describe in depth below, by limiting to a 12 hour sum window many mountain 

environments are under protected because the standard fails to include overnight/early morning 

exposures which can be high in mountains.

To fully protect vegetation from cumulative ozone and consideration of Class I areas that 

have peak ozone concentrations overnight, a full 24 hour standard is needed. The 2013 ISA 

recognizes the issue of higher nighttime concentrations stating: “Persistently high O3 

concentrations observed at many of the rural sites investigated here indicate that cumulative 

exposures for humans and vegetation in rural areas can frequently exceed cumulative exposures 

in urban areas.”525 Yet, EPA disregards overnight hours stating in the WREA that “Since plant 

and tree species are not photosynthetically active during nighttime hours, only O3 concentrations 

observed during daytime hours (defined as 8:00 AM to 8:00 PM local time) were included in the 

summations.”526 This is incorrect. A number of studies527 have shown that cumulative ozone 

exposure reduces stomatal control, amplifies water loss, and reduces tree growth. For instance, 

McLaughlin et al. (2007a) discuss that cumulative ozone exposure, including at nighttime, 

contributes to the physiological changes observed in tree species at mid-elevation locations in 

Great Smoky Mountain National Park. McLaughlin et al. shows evidence that ecosystem wide 

 

525 See ISA page 107. 

526 See U.S. EPA (2014). Welfare Risk and Exposure Assessment for Ozone, 4-6 [hereinafter WREA].

527 See e.g., S.B. McLaughlin et al. (2007). Interactive effects of ozone and climate on tree growth and water use in a 

southern Appalachian forest in the USA, New Phytologist, 174: 109-124; S.B. McLaughlin et al. (2007). Interactive 

effects of ozone and climate on water use, soil moisture content and streamflow in a southern Appalachian forest in 

the USA, New Phytologist, 174: 125-136; N.E. Grulke et al. (2004). Stomata open at night in pole-sized and mature 

ponderosa pine: implications for O3 exposure metrics, Tree Physiology.
202

impacts occur from cumulative ozone exposure detecting a reduction in late season stream flows 

from a forested watershed.528 

Sensitive species and elevated nocturnal ozone exposures co-occur. Of the 267 National 

Parks that are known to have ozone sensitive plants 226 parks have at least one species that has 

been documented to show nocturnal conductance (Alnus rugosa, Populus tremuloides, Pinus 

ponderosa, Pinus radiata, Fraxinus pennsylvanica, Liriodendron tulipifera and Prunus 

serotina). Further, we provide evidence of the nocturnal ozone exposures for a number of 

National Parks and other protected lands at both high and mid-elevation monitoring sites in 

Table 28. While we understand that other factors, such as turbulence, are important for ozone 

flux into plants, there are studies that have demonstrated ozone uptake and injury from nighttime 

exposures.

529 We believe the following combined factors should be considered by the 

Administrator, reflecting how a 12-hr only standard is only a conservative estimate of ozone 

exposure: 

 Many Class I areas have ozone sensitive species that also exhibit nocturnal conductance

 High overnight ozone levels can coincide with the presence of these species

 Ozone exposure can reduce some plants ability to control stomatal opening and closing 

and their overall response rate to stress 

 The main anti-oxidant defensive compound, ascorbate, is produced largely in daytime, 

due to photo dependent enzymatic activity. As it is depleted in late afternoon and into the 

night, it would leave plants less protected from nighttime and early morning elevated 

ozone concentrations

The ozone exposures are often significant for mountain sites, sites with daylight bringing 

rapid increases to mid-elevations as the overnight boundary layer breaks up, mixing ozone laden 

air to lower elevations and in evening as the boundary layer reforms and ozone that was formed 

over the day is transported to rural montane areas. Damage from ozone may be significant for 

mid-elevation area that see dramatic increases in morning time ozone levels from downward 

mixing of pollution aloft in combination in with mid-day local ozone production and evening 

transport events. The importance of the timing of elevated ambient ozone levels in relation to 

diurnal stomatal conductance and defensive anti-oxidant production has been discussed in the 

literature.

530

 

528 S.B. McLaughlin et al. (2007). Interactive effects of ozone and climate on water use, soil moisture content and 

streamflow in a southern Appalachian forest in the USA, New Phytologist, 174: 125-136

529 Winner et al. (1989). Plant responses to elevational gradients of O3 exposure in Virginia. Proc. Natl. Acad. Sci. 

USA Ecology Vol. 86 pp. 8828-8832; N.E. Grulke et al. (2004). Stomata open at night in pole-sized and mature 

ponderosa pine: implications for O3 exposure metrics, Tree Physiology; W.J. Massman (2004). Toward an ozone 

standard to protectvegetation based on effective dose: a review of deposition resistances and a possible metric, 

Atmospheric Environment 38: 2323–2337.

530 R.L. Heath et al. (2009). Temporal processes that contribute to nonlinearity in vegetation responses to ozone 

exposure and dose, Atmospheric Environment, 46: 2919-2928; R.C. Musselman et al. (2006). A critical review and 

analysis of the use of exposure- and flux-based ozone indices for predicting vegetation effects, Atmospheric 

Environment, 40: 1869–1888.
203

Table 28. Average % underestimation of monthly W126 12-hr summation window compared to 

24-hr by site. Includes 18 data points the months April – Sept. in the years 2006-2008. Original 

data from AQS & NPS, calculations by the Appalachian Mountain Club. 

LOCATION ELEVATION 

(M)

AVERAGE % 

UNDERESTIMATION 

(RANGE)

FEDERAL OR STATE 

PROTECTED LANDS

Mt. Washington Base 

(Camp Dodge) 452 25 (4 – 48)

White Mountain NF/ 

Appalachian Trail, 2 Class I 

Areas

Mt. Washington Summit 1910 55 (47 – 65)

White Mountain NF/ 

Appalachian Trail, 2 Class I 

Areas

Acadia- Cadillac Mtn. 466 45 (26 – 58) Acadia NP, Class I Area

Whiteface Base 625 55 (41 – 67) Adirondack State Park

Whiteface Summit 1480 59 (47 – 71) Adirondack State Park

Greylock Mountaina1140 48 (39 – 57) Appalachian Trail 

Blue Ridge Parkway-RO 675 9 (1 – 23) Blue Ridge Parkway

Blue Ridge Parkway-75 987 8 (1 – 18) Blue Ridge Parkway

Blue Ridge Parkway-FP 1585 62 (49 – 75) Blue Ridge Parkway

Shenandoah Big Meadow 1073 50 (42 – 56) Shenandoah NP, Class I Area

GSM Clingman’s Dome 2021 57 (48 – 64) Great Smoky Mtn NP, Class I 

Area

GSM Look Rock 793 48 (42 – 55) Great Smoky Mtn NP, Class I 

Area

GSM Cades Cove 564 14 (3 – 37) Great Smoky Mtn NP, Class I 

Area

Rocky Mountain Long's 

Peak 2743 29 (21 – 43) Rocky Mountain NP, Class I Area

Sequoia and Kings 

Canyon Ash Mountain 457 20 (8 – 29) Sequoia and Kings Canyon NP, Class I Area

Sequoia and Kings 

Canyon Lower Kaweah 1890 28 (21 – 44) Sequoia and Kings Canyon NP, Class I Area

Crestlineb1387 23 (11 – 29) San Bernardino National 

Forest

Yosemite Turtle Dome 1605 36 (27 – 48) Yosemite NP, Class I Area

a Greylock Mountain data missing April for 2007-2008 b Crestline data includes 2007-2009
204

5. A Standard of 75 ppb Is Not Protective of the Public Welfare 

In considering the protectiveness of the current standard we are very encouraged that the 

Administrator “recognizes the appropriateness and usefulness of the W126 metric.”

531 We also 

strongly agree with the Administrator’s opinion that the current standard of 75 ppb is not 

requisite to protect the public welfare and that revision is needed.532 The Administrator 

appropriately makes this judgment with particular attention to the sensitive vegetation and 

ecosystems in Class I areas and other public lands providing similar public welfare benefits. We 

also echo the Administrators reliance on the strong science base evidence around impacts to tree 

growth as well as the increased protection for carbon storage and other growth related effects. 

6. The Secondary Standard Must Be Set at a Level No Higher Than 7 

ppm-hrs 

a. Visible Foliar Injury 

EPA needs to protect against foliar injury in plants that benefit most with W126 values 

between 7 and 9 ppm-hrs, to protect the beauty and vitality of our National Parks and other 

public recreation lands. This level of protection is demonstrated in the WREA FIA/FHM 

analysis. Wetlands, which serve as important wildlife habitat, provide ecological diversity to 

landscapes, and often serve as important filters for soil contaminants, are especially at risk from 

the stress of foliar damage from ozone. 

Foliar injury due to ozone has long been used as a bioindicator of pollutant exposure and 

is a sign of plant stress as it signifies cellular death (See Exhibit 15). Bioindicator species are 

selected because of their sensitivity to ozone allowing for a visible evaluation of an area’s 

exposure. Foliar injury, with regard to indicating plant stress, is a public welfare impact as it 

demonstrates that the vegetation and ecosystem are experiencing ozone induced stress. Even in 

plants that don’t show actual injury, there is likely stress because they may have to either close 

stomates to protect against cell death which limits photosynthesis, or use carbon based 

antioxidant reserves to counter the ozone. While stress does not necessarily indicate that the tree 

or plant will actually be damaged the cumulative ozone stress over time, and the likely additional 

environmental stresses caused by air pollution, must be considered. Examples of likely cooccurring air pollution impacts include: short-term and long-term impacts of acid deposition533

, 

excess nitrogen inputs534, insect infestations535, and increased extreme precipitation events 

 

531 Proposed Rule at 75335. 

532 Id. at 75336.

533 N. Duarte et al. (2013). Susceptibility of Forests in the Northeastern USA to Nitrogen and Sulfur Deposition: 

Critical Load Exceedance and Forest Health, J. Water, Air, & Soil Pollution, 224; G.E. Likens & D.C. Buso (2012).. 

Dilution and the Elusive Baseline. Environ. Science & Technology, 46(8): 4382-4387.

534 C.M. Clark, et al. (2013). Estimated losses of plant biodiversity in the United States from historical N deposition 

(1985–2010), Ecology, 94:1441–1448. 

535 K.S. Knight et al. (2013). Factors affecting the survival of ash (Fraxinus spp.) trees infested by emerald ash borer 

(Agrilus planipennis) http://dx.doi.org/10.1007/s10530-012-0292-z
205

caused by climate change (including damaging icing events, floods, and increased frequency and 

severity of drought536).

Foliar injury also has another specific public welfare impact: its obvious degradation of 

aesthetics especially on public lands which are visited for sightseeing and recreation and are 

valued for beauty and healthy ecosystems. A recent summary of National Parks visitor 

surveys537 found that 88% and 90% of respondents found clean air and scenic views, 

respectively, to be extremely important or very important. Both features were most often in the 

top 2 ranked attributes that visitors value. 

EPA wrongly asserts there is ”a lack of guidance for federal land managers regarding 

what spatial scale or degree of severity of visible foliar injury is considered sufficient to trigger 

protective action for O3 sensitive AQRVs.”538 The National Park Service has provided guidance 

in a 2011 document539 that it views W126 exposures greater than 7 ppm-hrs to represent 

moderate to major impacts on ozone-sensitive vegetation (including foliar injury). The Park 

Service based this view in part on the findings of an expert workgroup that a W126 of 5–9 ppmhrs would protect plants in natural ecosystems against foliar injury. More importantly, in 

comments to EPA, the National Park Service has repeatedly called for a secondary standard in 

the 7 to 9 ppm-hrs range based in part on concerns about ozone-induced foliar injury540. Thus 

EPA is simply wrong in asserting that there is a lack of guidance from federal land managers 

regarding the degree of ozone-induced foliar injury warranting protective action.

EPA’s proposal is unprecedented in that it eliminates the use of foliar injury to inform the 

level of W126 that would be protective under a national welfare standard. EPA wrongly asserts 

in its proposal that CASAC provided no guidance on foliar injury benchmarks541 as they did for 

biomass loss and crop yields. This is false. CASAC frames it’s overall recommendation of 7-15 

ppm-hrs on the basis of all the evidence of casual effects to vegetation including the foliar injury 

information.

542 In CASAC’s comments on the second draft Policy Assessment they explicitly 

state: “A level below 10 ppm-hrs is required to reduce foliar injury.” (emphasis added).

This is consistent with the CASAC committee’s consensus comments on the draft WREA 

where they clearly point to the significance of the USFS FHM/FIA ozone biomonitor data and 

the level of 10 ppm-hrs as an upper bound for foliar injury.

Figures 7-9 and 7-11, showing the cumulative number of biosites with any injury as a 

function ofW126, are very clear and effective in communicating the risk due to ozone. 

 

536 W.R. L. (2013). Consequences of widespread tree mortality triggered by drought and temperature stress, Nature 

Clim. Change, 3:30–36 http://dx.doi.org/10.1038/nclimate1635

537 National Park Service (2013). Natural Resource Stewardship and Science, available at

https://psu.uidaho.edu/files/vsp/reports/5003_NPS_rept_2013.pdf. 

538

 National Park Service (2011). Technical Guidance on Assessing Impacts to Air 

Quality in NEPA and Planning Documents, see 13-14, Guidance available at 

http://www.nature.nps.gov/air/Pubs/pdf/AQGuidance_2011-01-14.pdf

539 Id.

540 NPS Letter N3615 (2301) Oct. 5th, 2007, NPS Letter N3615 (2350) March 20th, 2014.

541 Proposed Rule at 75,334

542 CASAC Letter 2014a at iii. 
206

This analysis also reveals a change in the E-R slope near 10 ppm-hrs. However, this slope 

change is not a threshold for no injury. Based on this E-R slope change, 10 ppm-hrs is a 

reasonable candidate level for consideration in the WREA, along with other levels.”.

543

Figure 14. EPA WREA figure 

showing the cumulative 

proportion of sites with foliar 

injury present, by moisture 

category. Note that reductions in 

the proportion of sites, in each 

moisture category, largely occur 

below a W126 of 10 ppm-hrs.

 

543 Letter from CASAC Chair Dr. H. Christopher Frey to U.S. EPA Administrator Gina McCarthy, re: CASAC 

Review of the EPA’s Welfare Risk and Exposure Assessment for Ozone (Second External Review Draft) ( EPACASAC-14-003), 7, June 18, 2014.
207

EPA relies on a misguided rationale that the variability of foliar injury response and the 

difficulty in identifying an alternative level of the standard make it too challenging to assess. 

EPA states: “Thus, while the PA recognizes visible foliar injury as an important O3 effect which, 

depending on severity and spatial extent may reasonably be concluded to be of public welfare 

significance, most particularly in nationally protected areas such as Class I areas, it additionally 

recognizes the appreciable variability in this endpoint, which poses challenges to giving it 

primary emphasis in identifying potential alternative standard levels.” Variability should in no 

way discount the positive observations of foliar injury and its relationship with a W126 level. A 

recent example is Kohut et al. 2012 who found that the W126 3-month form was a consistent 

predictor of ozone foliar injury on cutleaf coneflower (Rudbeckia laciniata var. ampla) over 5 

years in Rocky Mountain National Park. 544 

EPA’s review of the FIA/FHM dataset provides a clear relationship between the W126 

and foliar injury when sites that showed positive injury are sorted by soil moisture. This 

relationship is significant in that it allows land managers to recognize the W126 levels that can 

cause foliar damage that is not only unsightly to the public but also indicates plant stress. The 

high variability in foliar injury occurrence should not negate the positive findings where a robust 

relationship with W126 can be found. These positive findings necessitate action by EPA to 

protect the public welfare from the impacts that they represent. 

To the extent EPA is suggesting that it can deem visible foliar injury as not being an 

adverse effect on welfare, such a suggestion is unlawful and arbitrary. EPA itself has repeatedly 

identified foliar injury as adverse effects in prior reviews.545 In its 2010 reconsideration 

proposal, EPA stated: “In an area such as a national park, where visitors come in part for the 

aesthetic quality of the landscape, the Administrator recognizes that visible foliar injury 

incidence is an important welfare effect which should be considered in determining an 

appropriately protective standard level.546 On the same page, EPA also said the 1996 consensus 

workshop findings (which, among other things, recommended levels of protection against foliar 

injury) should be given substantial weight.547 And the 2010 proposal went on to say:

The Administrator also believes that in order to preserve wilderness areas in an 

unimpaired state for future generations, she must consider a level that affords 

substantial protection from known adverse O3-related effects of biomass loss 

and foliar injury on sensitive tree species, as well as a level that takes into 

 

544 R. Kohut (2012) Foliar Ozone Injury on Cutleaf Coneflower at Rocky Mountain National Park, Colorado, 

Western North American Naturalist, 72(1)” 32-42.

545 See, e.g., 73 Fed. Reg. 16,496/2,: “[T]he Administrator finds that evidence that has become available in this 

review demonstrates the occurrence of adverse vegetation effects at ambient levels of

recent O3 air quality, and that evidence and exposure- and risk-based analyses indicate that adverse effects would be 

predicted to occur under air quality scenarios that meet the current standard, taking into consideration both the level 

and form of the current standard. Ozone exposures that would be expected to remain after meeting the current 

secondary standard are sufficient to cause visible foliar injury and seedling and mature tree biomass loss in O3-

sensitive vegetation.”; id. at 16490/3 (“Staff Paper concluded that the current standard continues to allow levels of 

visible foliar injury in some locations that could reasonably be considered to be adverse from a public welfare 

perspective”).

546 75 FR at 3,025.

547 Id.
208

account potential ‘‘anticipated’’ adverseO3-related effects, including effects that 

result in continued impairment in the year following O3 exposure (i.e., carryover 

effects).548

Further, CASAC specifically identified visible foliar injury as an adverse welfare effect, 

as did the PA.549 EPA offers no reasoned basis for rejecting these conclusions. 

EPA asserts550 that its refusal to protect against visible foliar injury is justified in light of 

“the significant challenges in judging the extent to which such effects should be considered 

adverse to the public welfare, in light of the variability and the lack of clear quantitative 

relationship with other effects on vegetation, as well as the lack of established criteria or 

objectives that might inform consideration of potential public welfare impacts related to this 

vegetation effect.” Not only do these assertions lack rational support for the reasons specified 

above, but the rationale they reflect is essentially the same as the one rejected by the Court in 

American Farm Bur. Fd. v. EPA, 559 F.3d 512, 530 (D.C. Cir. 2009). There, EPA refused to 

specify a level of welfare protection for visibility because of the allegedly subjective nature of 

the value. The Court held EPA’s refusal was unlawful and arbitrary:

The EPA's assertion that it need not determine what level of visibility protection 

is requisite to protect the public welfare fails under the plain language of the 

statute. The CAA provides: “Any national secondary ambient air quality standard 

shall specify a level of air quality the attainment and maintenance of which ... is 

requisite to protect the public welfare from any known or anticipated adverse 

effects....” 42 U.S.C. § 7409(b)(2) (emphases added). The EPA's failure to 

identify such a level when deciding where to set the level of air quality required 

by the revised secondary fine PM NAAQS is contrary to the statute and therefore 

unlawful. Furthermore, the failure to set any target level of visibility protection 

deprived the EPA's decision making of a reasoned basis. Because the EPA failed 

to identify any target level, we need not decide whether it was reasonable for the 

agency to reject the target recommended by the Staff Paper and the CASAC 

because it was based on uncertain subjective evidence

Under the same reasoning, EPA cannot forego identifying a level of protection against 

foliar injury that is requisite to protect against adverse effects on public welfare, and setting a 

level of air quality to provide that level of protection – notwithstanding EPA’s claims of 

difficulty in identifying such levels of protection.

Finally, CASAC and the PA were both clear that W126 values below 10 ppm-hrs are 

required to reduce the number of sites showing such injury – there was no material uncertainty 

cited on this point. CASAC further stated that the 10 ppm-hrs figure was based on its scientific 

 

548 Id. at 3,025-26 (emphasis added)

549 Letter from CASAC Chair Dr. H. Christopher Frey to U.S. EPA Administrator Gina McCarthy, re: CASAC 

Review of the EPA’s Welfare Risk and Exposure Assessment for Ozone (Second External Review Draft) ( EPACASAC-14-003), 7, June 18, 2014; Policy Assessment at ES-8, 5-51, 5-52. 

550 Proposed Rule at 75349.
209

judgment.551 Accordingly, EPA must adopt a standard at least as protective as 10 ppm-hrs unless 

EPA can articulate a fully sufficient scientific basis for rejecting CASAC’s advice. See Part 

V.C. above. EPA has failed to articulate any such basis in the record here. 

b. Tree biomass; growth and productivity 

CASAC has identified a 2% biomass loss as “an appropriate scientifically based value to 

consider as a benchmark of adverse impact for long-lived perennial species such as trees, 

because effects are cumulative over multiple years.”552 EPA does not offer a scientifically based 

or otherwise rational basis for concluding otherwise. Further, as CASAC found the level of 7 

ppm-hrs is the only level analyzed for which the relative biomass loss for the median tree species 

is less than or equal to 2%.553 Accordingly, EPA must protect against tree biomass loss greater 

than 2% annually by adopting a W126 level of 7 ppm-hrs to protect forests and ecosystems, 

especially in Class I areas. The WREA and other material in the record provides clear evidence 

that tree biomass loss increases with increasing W126 levels above 7 ppm-hrs based on 

concentrations exposure response curves. Further, sensitive tree species, that experience 

significant biomass loss when exposed to ozone, are integral to our nation’s forest and even 

urban/suburban landscaping and greenways. 

EPA incorrectly reasons that an upper level of the W126 for protecting tree biomass loss, 

as relative biomass loss, should be 17 ppm-hrs because this aligns with CASAC comment that 

>6% biomass is unacceptably high and because 17 and 15 (CASAC recommended upper limit) 

have the same median percent loss (5.3%). Further, EPA purports that there is little difference 

from 17 down to 9 ppm-hrs because there is no change in the number of tree species at or below 

2% biomass loss, e.g. 5 out of 11. However, there are some very serious deviations between 

EPA’s rationale and that of CASAC.

1. CASAC % loss judgments are based on an annual form of the W126 standard, yet EPA is 

proposing a 3 year averaging.

2. CASAC puts the most weight on the median % biomass loss, values that DO CHANGE 

dramatically over the same range that EPA says there is no difference (with 5/11 species). 

3. CASAC clearly supports 7 ppm-hrs as appropriate to protect trees from significant 

biomass loss, at no greater than 2%, while EPA wrongly construed CASAC comment to 

indicate that 6% biomass loss is acceptable. Moreover, CASAC’s rejection of 17 ppmhrs as the top of the range was not based solely on the assumption of a 6% biomass loss 

at that level. CASAC also relied on evidence of adverse effects at 10 and 7 ppm-hrs.554

One CASACs’ member provides more context in his individual comments where he 

states: 

“We favor using a measure of central tendency of the data, specifically the 

median across species (the green line in Fig. 5-2). This analysis provides the median of 

best available estimates within each species, and the median across species with all 

 

551 CASAC Letter 2014a at 15. 

552 Id. at 14. 

553 Id. 

554 Id. at 12.
210

species treated equally. Table 6-1 presents the RBL results for individual species for 

different levels of W126. This table demonstrates that a range of 7 ppm-hrs to 15 ppm-hrs 

will protect against RBL of 2% for at least 5 of the 12 species. We do not consider a 

value of 17 ppm-hrs from Table 6-1 because even though only 5 of 12 tree species are 

estimated to have relative biomass loss of 2 percent or less at this level, the median 

species has relative biomass loss of 6.0 percent, which is unacceptably high. With 

compounding over the harvest cycle or life span of these species, this will result in 

considerably greater cumulative RBL as discussed above. For the more sensitive tree 

seedlings, a value closer to the lower end of the range (7 ppm-hrs) would be more 

appropriate. The level of 7 ppm-hrs is the only level analyzed for which the relative 

biomass loss for the median tree species is less than or equal to 2 percent.”555

EPA must not misconstrue the reasoning and position of CASAC when making a 

final decision on the secondary standard. Instead the Agency must consider the science 

squarely and set a W126 secondary standard to 7 ppm-hrs to protect tree growth and health 

and thereby public welfare. 

c. Increase protection of carbon storage; benefits to climate 

change

The Administrator has specifically pointed to the fact that reduction of carbon storage is 

important public welfare harm from ozone, providing an important rationale for the need to 

revise the current standard.556 This is supported in the recent ISA that cites consistent findings of 

carbon loss with ozone damage.557 EPA estimates that transitioning to a W126 of 7 ppm-hrs 

would reduce carbon dioxide equal to taking 11 million cars off the road via increased carbon 

sequestration558. EPA qualifies this estimate as likely low, as their analysis did not include the 

forests on public lands, therefore the climate benefits are likely much greater. Given EPA’s 

identification of the importance of ozone’s negative impacts on vegetative carbon storage, such 

an impact plainly qualifies as an adverse welfare effect. Yet EPA does not even attempt to 

protect against the degree of such effects predicted to occur at levels below 13 ppm-hrs (and its 

proposal does not even assure protection at the 13 ppm-hrs level, given the agency’s proposed 

use of 8-hour standards that – as demonstrated above- are not as protective as the W126 levels 

under consideration.). 

EPA fails to rationally explain its failure to identify or provide requisite protection levels 

against this important welfare impact. At one point, the agency seeks to minimize the 

significance of additional carbon storage that would be provided with more protective W126 

levels. EPA asserts that as a percent of the estimated carbon storage under the current standard, 

estimates of storage over 30 years under the 15, 11 and 7 ppm-hrs scenarios are less than 0.1% 

(13 MMtCO2e), just under 1% (593 MMtCO2e) and under 2% (1,600 MMtCO2e).559 But by 

EPA’s own measures, 1,600 MMt over 30 years (estimated at the 7 ppm-hrs levels) is actually 

 

555 Id. at 14 (emphasis added).

556 Proposed Rule at 75315/2, 75321/1, 75336.

557 Id . at 75,315/1.

558 WREA.

559 Proposed Rule at 75,325/2. 
211

very significant. By comparison, EPA's projections for its Clean Power Plan (i.e., setting 

standards of performance for carbon emissions from existing power plants under CAA §111(d) 

are that it will reduce CO2 emissions by roughly 300-500 MMt per year.560 So the carbon 

reduction benefits of a 7 ppm-hrs ozone standard over 30 years would be very roughly equal to 

about 4 years of the benefits from EPA’s Clean Power Plan. EPA can hardly claim that such 

benefits are insignificant from a public welfare perspective.

7. A Range of 13 to 17 ppm-hrs Does Not Assure Requisite Protection

To justify its proposal to set the secondary standard within the same range as the primary, 

EPA uses a range of 13- 17 ppm-hrs as a basis for comparison. Use of such a range does not 

assure requisite protection against the adverse effects on public welfare for the following 

reasons:

i) The range is contrary to the advice of both CASAC and PA that the lower bound of the 

range be 7 ppm-hrs; and contrary to CASAC’s advice that the upper bound be no higher than 15 

ppm-hrs.561 EPA fails to fully or rationally explain its rejection of CASAC and PA advice on the 

range. EPA offers an unsupported claim that there is greater uncertainty as to extent to which 

estimates of benefits in terms of ecosystem services and reduced effects on vegetation at lower 

levels might be judged significant to public welfare. But CASAC expressly cautioned against 

over-emphasis on uncertainty at levels below 15 ppm-hrs, finding that plant injury is clearly 

observed at and well below that level.562 CASAC also expressly found that “there is quite a lot of 

certainty in estimates of biomass loss for forest tree seedling species for which E-R functions 

have been developed.563 It further found that “based on scientific judgment of CASAC...7 ppmhrs is protective of relative biomass loss for trees....and is protective of ecosystem services.”564

And CASAC found that “[f]or the more sensitive tree seedlings, a value closer to the lower end 

of the range (7 ppm-hrs) would be more appropriate. The level of 7 ppm-hrs is the only level 

analyzed for which the relative biomass loss for the median tee species is less than or equal to 2 

percent.”565 EPA provides no scientific or reasoned basis for differing from these scientific 

CASAC and PA findings.

ii) EPA cites566 the WREA’s alleged showing of “relatively small additional benefits and 

increased uncertainty with the ecosystem services estimates” in the scenarios at and below 11 

ppm-hrs. EPA claims that the PA observes similarity in the number of species with less than 2% 

RBL across the range from 17 to 9 ppm-hrs. The agency also claims that a similar number of 

species have RBL estimates below 5% for values of 13 and 11. In reality, there are significant 

differences in the number of species with RBL below 5% at different W126 levels. Table 29567

 

560 See 79 Fed. Reg. 34,830, 34,931-33 (2013).

561 EPA also wrongly suggests that CASAC purportedly endorsed 13 ppm-hrs, when in fact CASAC simply gave it 

as an example of how EPA might translate a one-year W126 standard of 15 to a 3-year average standard: CASAC 

did not in fact endorse such an approach: It was absolutely clear that CASAC advised a single year standard.

562 CASAC Letter 2014a at 12. 

563 Id. at 5. 

564 Id.

565 Id. 14. 

566 Proposed Rule at 75,349/2.

567 Id. at 75430)
212

shows 5 species with RBL less than 5% at 17 ppm-hrs; 8 at 11 ppm-hrs; and 10 at 9 ppm-hrs 

(double the number at 17). Even as between 13 and 11 ppm-hrs, there is 1 additional species

showing less than 5% RBL at 11: And given that the analysis only looked at 11 species, one 

additional species represents 9% of the species – hardly trivial. Further, discounting the impact 

on even just one species conflicts sharply with EPA’s stated intent to focus particular 

significance on adverse effects that occur on sensitive species.568 

Likewise, EPA asserts that there is similarity in the number of species with less than 2% 

RBL across the W126 range from 17 to 9 ppm-hrs. While it’s true the same number of species 

(5) suffer less then 2% RBL throughout that range, it’s also the case that the median species has 

more than double the loss at 17 than it does at 9 (5.3% versus 2.4%) – and throughout the 9-17 

range there is a steady increase in the medial species loss.569 It is therefore arbitrary to imply that 

17 provides equivalent protection. 

iii) EPA wrongly suggests (79 Fed. Reg. at 75348/3) that CASAC rejected 17 ppm-hrs as 

the top of the range only because it assumed that the RBL at that level would be 6% - a number 

that was later reduced to 5.3% in the final PA. But CASAC’s rejection of 17 was not based 

solely on the assumption of 6% biomass loss at that level. CASAC also relied on adverse effects 

that occur at 10 and 7 ppm-hrs.570 

iv) EPA also rejects CASAC and PA recommendations for 7 ppm-hours as the lower end 

of the range on the grounds that CASAC’s recommendation was a policy one, that there is 

greater uncertainty on the extent to which estimated benefits in terms of ecosystem services, and 

reduced effects on vegetation at lower ozone exposures, might be judged significant to public 

welfare, and on grounds of alleged relatively small additional benefits in ecosystem services at 

lower levels.571 These assertions are baseless. CASAC expressly said its recommended range 

was scientifically based.572 These recommendations are based on scientific evidence of adverse 

effect associated with the presence of ozone in ambient air. Note that these levels are based on an 

annual form of the standard. In reaching its scientific judgment regarding the indicator, form, 

averaging time, and range of levels for a revised secondary standard, the CASAC has focused on 

the scientific evidence for the identification of the kind and extent of adverse effects on public 

welfare.”). Because CASAC’s advice was expressly based on scientific conclusions, EPA must 

provide more than assertions of uncertainty to depart from CASAC’s judgment: It must provide 

a full and reasoned scientific rationale: The agency has failed to do so here.

EPA also has no reasoned basis for claiming greater uncertainty as to welfare benefits at 

lower levels: As noted above, CASAC expressly cautioned against overstating such uncertainty, 

found “quite a lot” of certainty in the estimates of biomass loss, and expressly relied on those 

estimates to recommend 7 ppm-hrs as the low end of the range. 

 

568 Proposed Rule at 75,348/1, 2.

569 Id. at 75,340. 

570 CASAC Letter 2014a at 12.

571 Proposed Rule at 75,349/2. 

572 E.g., CASAC Letter 2014a at iii, 14 (“In our scientific judgment, it is appropriate to identify a range of levels of 

alternative W126-based standards that includes levels that aim for not greater than 2% RBL for the median tree 

species.”); id. at 15 (“(3) the level of the standard should be between 7 ppm-hrs and 15 ppm-hrs.
213

Finally, EPA’s claim of relatively small additional benefits at lower W126 levels is 

refuted in subparagraph d.ii above. 

8. EPA’s Proposal Fails to Specify Requisite Levels of Vegetation 

Protection as Required by the Act

The Act requires EPA to “specify a level of air quality the attainment and maintenance of 

which ... is requisite to protect the public welfare from any known or anticipated adverse 

effects.” 42 U.S.C. §7409(b)(2). The Farm Bureau Court held that this language requires EPA 

to first identify the requisite level of protection for the affected welfare value (there, visibility), 

and then set the secondary NAAQS to achieve that level of protection. 559 F.3d at 529-30. 

“EPA’s failure to identify such a level when deciding where to set the level of air quality 

required by the revised secondary ... NAAQS is contrary to the statute and therefore unlawful. 

Furthermore, the failure to set any target level of visibility protection deprived the EPA’s 

decisionmaking of a reasoned basis.” Id. 530. 

In reviewing EPA’s 2008 ozone NAAQS decision, the D.C. Circuit held that EPA had 

again failed to comply with §7409(b)(2) as construed in Farm Bureau. There, EPA adopted a 

secondary standard identical to the primary without specifying a level of protection of vegetation 

requisite for public welfare. The Court said:

EPA's explanation for setting the secondary standard identical to the primary 

standard fails under American Farm Bureau. As we explained there, it is 

insufficient for EPA merely to compare the level of protection afforded by the 

primary standard to possible secondary standards and find the two roughly 

equivalent. EPA must expressly “determine what level of ... protection is requisite 

to protect the public welfare,” American Farm Bureau, 559 F.3d at 530, and 

explain why this is so. Here EPA found “significant overlap” between the revised 

primary standard and “selected levels” of a seasonal standard, 2008 Final Rule, 73 

Fed.Reg. at 16,499, and it did say that the revised primary standard “would be 

sufficient to protect public welfare from known or anticipated adverse effects,” id.

at 16,500. But it justified this conclusion only by comparing the revised primary 

standard to a seasonal level of 21 ppm-hours that EPA never “specif[ed]” was 

“requisite to protect the public welfare,” 42 U.S.C. § 7409(b)(2)—exactly what 

American Farm Bureau held is inconsistent with the statute.

. . . 

Because EPA failed to determine what level of protection was “requisite to 

protect the public welfare,” EPA's explanation for the secondary standard violates 

the Act. We therefore remand this portion of the final rule for further explanation 

or reconsideration by EPA.

Mississippi, 744 F.3d at 1360-62. 
214

EPA’s proposal fails to comply with the Act and the Court’s remand order. The agency 

has completely failed to identify target levels of vegetation protection requisite for protection of 

public welfare and specify levels of air quality that will achieve that protection. Although the 

proposal discusses various potential levels of tree growth and crop impairment from ozone, and 

thresholds identified by CASAC for protection against such impacts, no where does it specify 

levels of protection that the agency itself proposes as requisite levels of protection against these 

adverse welfare impacts. And as already noted, the agency also fails to propose a requisite level 

of protection against foliar injury. 

EPA does identify a range of 13 – 17 ppm-hrs, but that range is not based on any 

proposed level of protection against biomass loss, carbon storage loss, or foliar injury that EPA 

has identified as requisite for public welfare. EPA notes CASAC’s views that a 2% biomass loss 

is protective and a 6% loss level is unacceptable, but refuses to specify what level of protection 

EPA itself proposes to find requisite. Accordingly, under the holdings of Farm Bureau and 

Mississippi, EPA’s proposal violates the Act and is arbitrary.

Likewise, EPA’s proposal to set the secondary standard identical to the primary is based 

on the same sorts of comparative analyses rejected in Farm Bureau and Mississippi. That air 

quality in some (or even many) areas that meet the proposed primary standards might also meet 

various levels of a W126 standard does not show either that the W126 levels evaluated reflect 

levels requisite to protect welfare, or that the primary standards will assure achievement of such 

levels of protection. 

Finally, even if not otherwise unlawful and arbitrary, EPA’s proposal to set the secondary 

standard as identical to primary when the agency does not even know the level at which the final 

primary standard will be set renders the proposal arbitrary and unlawful. The Act requires EPA 

to set the primary standard to achieve a different objective than the secondary: the protection of 

public health with an adequate margin of safety. The notion that the level chosen to protect 

public welfare will just by happenstance be the very same level requisite to protect public 

welfare is arbitrary and not credible. EPA must specify the level for the secondary standard 

based on what is requisite to protect public welfare against adverse welfare impacts – here 

damage to forests, trees and crops. EPA’s basis for choosing of a given level to protect health 

cannot also provide a rational basis for protecting vegetation. 

9. Air Quality Monitoring Requirements

a. Changes to length of monitoring seasons 

We support an extended monitoring season for the secondary standard that reflects 

regional seasonal differences in the growing season. Photosynthesis in conifers and early 

emerging forest floor species begins before deciduous canopy leaf-out which should be 

considered in setting the length of the monitoring season. Further, the growing season can vary 

greatly across the U.S. EPA also must account for the extended timing of elevated ozone 

concentrations in the context of climate change. 

b. Need for more monitors in rural and mountain areas
215

We are concerned that EPA is not taking the necessary steps to ensure that monitoring 

will be adequate to effectively implement any new secondary standard. EPA has long 

acknowledged that uncertainties will remain about ozone concentrations affecting sensitive 

natural vegetation and ecosystems until additional monitors are sited in National Parks 

wilderness areas and other public lands. Yet EPA does not propose to address these concerns. 

EPA should identify monitoring needs in parallel to finalizing this proposal. EPA has the 

information necessary to identify ecosystems of concern for impacts from ozone and plan an 

appropriate distribution of monitors. This information should be used to outline the monitoring 

that will be required to protect these areas. 

Moreover, while additional monitors are of great importance it is critical that existing 

monitors be maintained. Funding cuts in recent years have led to the removal of important 

monitors. Monitored data is the lifeblood of NAAQS and EPA should ensure that funding for 

monitors be a priority for the agency. 

10. SIP Requirements

a. Attainment Schedule for Secondary Standards Must be 

Expeditious

The attainment of the secondary standards must be done in compliance with Clean Air 

Act section 172. (a) (2) (B) which states: “The attainment date for an area designated 

nonattainment with respect to a secondary national ambient air quality standard shall be the date 

by which attainment can be achieved as expeditiously as practicable after the date such area was 

designated nonattainment under section 7407(d) of this title. ”

While the CAA does not provide the same timeline for attainment for the secondary 

standards as it does the primary standards, it nonetheless requires action that is as expeditious as 

practicable. EPA must require states to clearly define this timeline in their SIPs. 

G. It is Critical For EPA To Set The NAAQS At A Truly Health Protective 

Level To Allow People To Engage In Protective Behavior When The Air 

Quality Index, Which Is Keyed To The NAAQS, Alerts Them That Safe 

Levels Of Ozone Have Been Exceeded 

The importance of setting the Ozone NAAQS at a health-protective level of no higher 

than 60 ppb is further underscored by the fact that the NAAQS are directly tied to the Air Quality 

Index (“AQI”) and therefore critical to the public’s ability to engage in so-called averting 

behavior, i.e. behavior to reduce their exposure to ozone.573 If the NAAQS are not set at a truly 

health-protective level, the AQI will not serve its purpose of informing the public about how 

 

573 Averting behavior typically includes reducing time spent outdoors or reducing the level or duration of outdoor 

activity during times of the day when ozone levels are high. 
216

clean or polluted the air is and people will be denied the opportunity to protect themselves and 

their children from unhealthy air. 

1. The AQI Must Accurately Inform the Public of Health Hazards From 

Polluted Air

a. The Primary Purpose of the AQI Is to Facilitate Averting 

Behavior

The AQI is an EPA-administered, nationally uniform index for reporting and forecasting 

daily air quality. Its very purpose is the dissemination of accurate air pollution information. The 

AQI for ozone574 runs from 0 to 500, with higher AQI values corresponding with greater levels 

of air pollution and greater health concerns. For ease of reference, the ozone AQI is divided into 

six color-coded categories, each of which corresponds to a different level of health concern: 

Air Quality Index

(AQI) Values Levels of Health Concern Colors

When the AQI is in this 

range:

..air quality conditions are: ...as symbolized by this 

color:

0-50 Good Green

51-100 Moderate Yellow

101-150 Unhealthy for Sensitive 

Groups Orange

151 to 200 Unhealthy Red

201 to 300 Very Unhealthy Purple

301 to 500 Hazardous Maroon

Green: Air quality is considered satisfactory, and air pollution poses little or no risk.

Yellow: Air quality is acceptable; however, for some pollutants there may be a moderate 

health concern for a very small number of people. For example, people who are unusually 

sensitive to ozone may experience respiratory symptoms.

Orange: Although general public is not likely to be affected at this AQI range, people 

with lung disease, older adults and children are at a greater risk from exposure to ozone, 

whereas persons with heart and lung disease, older adults and children are at greater risk 

from the presence of particles in the air. . 

Red: Everyone may begin to experience some adverse health effects, and members of the 

sensitive groups may experience more serious effects. .

Purple: This would trigger a health alert signifying that everyone may experience more 

serious health effects.

 

574 EPA also calculates the AQI for four other major air pollutants regulated by the Clean Air Act: particle pollution 

(also known as particulate matter), carbon monoxide, sulfur dioxide, and nitrogen dioxide.
217

Maroon: This would trigger health warnings for emergency conditions. The entire

population is more likely to be affected.575

Under the proposed revision, an AQI value of 100 would correspond with the revised ozone 

NAAQS, i.e. the level set by EPA to protect public health. Accordingly, when AQI values are 

below 100, EPA encourages the public to consider air quality as generally healthy, while when 

AQI values are above 100, the public is cautioned to consider air quality as unhealthy, first for 

certain sensitive groups of people, and eventually, as AQI values get higher, for the entire 

population.576

Accordingly, a primary function of the AQI is to notify the public about when ozone 

levels are or are expected to be high, in order to give people the opportunity to reduce their 

exposure to ozone through so-called averting behavior. To that end, the AQI is widely 

disseminated: it can be found on the internet (on the EPA-developed AIRNow website as well as 

many weather reporting websites), in local and national media (including USA Today, The 

Weather Channel, and CNN), and through EnviroFlash, a free e-mail alert system that sends 

daily air quality forecast to its subscribers.577

b. AQI Values Are Widely Disseminated Through a Robust 

Infrastructure 

In addition to the AQI’s generally wide dissemination through media and internet outlets, 

state and local actors--including schools, community organizations, and city, county and state 

agencies and governments--have also developed a robust infrastructure whose aim is to broadcast 

AQI values and the attendant public health information to the public. Most notably, this 

infrastructure includes air alert programs, which were established to warn residents when levels 

of air pollution reach unhealthy levels and which are currently operated by hundreds of cities and 

air pollution control agencies across the country. Alert days,578 which can be declared by a local 

municipality, county or state, are typically set when air quality enters the unhealthy ranges, i.e. 

when the AQI exceeds 100. When an alert is issued, the issuing agency directly contacts a set list 

of recipients, including local schools, TV stations and newspapers. According to the most recent 

information provided by the EPA, at least 292 cities in 35 states participate in air quality alert 

days.579 Another widely implemented program is the School Flag Program, through which 

schools are alerted to the local air quality forecast and instructed to take steps to protect students’ 

health from air quality hazards. The program requires schools to raise a flag that corresponds to 

each day’s air quality, with the flag color matching the AQI colors. On unhealthy air days, 

schools use the air quality information to encourage averting behavior in order to reduce 

students’ exposure to air pollution. Thus, for example, schools might adjust physical activities on 

unhealthy air days by either shortening, cancelling or moving outdoor activities indoors, or they 

might require teachers to take longer breaks during athletic activity or ensure that asthma quick-

 

575 U.S. EPA, Air Quality Index (AQI)—A Guide to Air Quality and Your Health, available at

http://www.epa.gov/airnow/aqi_brochure_02_14.pdf.

576 See id.

577 Id.

578 Also called Ozone Action Days, Clean Air Alert, and Air Quality Alert, among others. 

579 See U.S. EPA, AIRNow Home: Action Days, available at 

http://www.airnow.gov/index.cfm?action=airnow.actiondays (accessed Feb. 19. 2015).
218

relief medicine is on hand. According to the most recent information provided by the EPA, at 

least 551 schools in 29 states participate in the School Flag Program.580

c. The AQI Is Relied On By Large Numbers of the Population.

The information provided by the AQI is important to and relied on by large portions of 

the public, as evidenced by multiple studies showing widespread and significant averting 

behavior in response to air quality advisories. For example, a national study analyzing air-quality 

alert programs found that on average, individuals reduce the time they spend in vigorous outdoor 

activities by 18% on air-quality alert days, and are 3% less likely to participate in any vigorous 

outdoor activities on alert days.

581 An earlier study investigating whether individuals varied 

outdoor activities in response to air-quality alerts found that that 40% of respondents stayed 

indoors on poor-quality air days and that individuals with smog-related symptoms significantly 

reduced time spent outdoors (shortening outdoor activities by about 40 minutes) when ozone 

concentrations exceeded the national standard.582 A study of data at outdoor facilities in the Los 

Angeles area showed significant pollution-avoidance behavior, with attendance dropping by as 

much as 15% on air-quality alert days.583

Studies also show that averting behavior is particularly pronounced among sensitive 

populations, such as children, the elderly and those with respiratory illnesses.584 For example, a 

survey of parents at a pediatric clinic found that 88% of parents were aware of air pollution 

advisories, 71% reduced pollution and 55% sometimes restricted children’s play because of 

advisories.585

d. The Air Quality Index is Used to Reduce Emissions as Well, 

And Requires the Concentration that Triggers Actionable 

Thresholds Be Set at Much Lower Levels

The Air Quality Index not only provides information to the public that will allow them to 

reduce their exposure to ozone as described above, the AQI also plays a critical role in the State 

Implementation Plans for meeting the ozone standard. That role requires that the EPA should 

strengthen certain key thresholds for the ozone AQI that trigger the emission reduction actions.

Many states have incorporated special actions on days when ozone levels were forecasted 

to reach higher levels in an effort to change behaviors or prevent emissions, in order to reduce 

the production of precursor emissions for ozone. For example, Utah has a system to alert 

 

580 U.S. EPA, School Flag Program Registered Schools, available 

athttp://www.airnow.gov/index.cfm?action=airnow.schoolflagprogramlist (accessed Feb. 19, 2015).

581 A.L. Sexton (Responses to Air Quality Alerts: Do Americans Spend Less Time Outdoors? (2011), available 

athttp://www.apec.umn.edu/prod/groups/cfans/@pub/@cfans/@apec/documents/asset/cfans_asset_365645.pdf.

582 See B. Bresnahan,, M. Dickie, & S. Gerking (1997). Averting Behavior and Urban Air Pollution, Land 

Economics, 73(3): 340-357 .

583 M.J. Neidell (2010). Information, Avoidance Behavior, and Health: The Effect of Ozone on Asthma 

Hospitalizations, J, of Human Resources, 44(2): 450-478. 

584 See, e.g., id. (noting that children and the elderly showed a greater response than adults); see also Sexton 2011.

585 M. McDermott, J. Srivastava, & S. Croskell (2006). Awareness of and compliance with air pollution advisories: 

A comparison of parents of asthmatics with other parents, J. of Asthma, 43: 235-239.
219

residents for high ozone days that breaks action into 3 categories586: Unrestricted action, 

Voluntary Action and Mandatory Action which requires employers to limit driving by their 

employees. The timing for these actions depends on the AQI forecast. Likewise, Washington 

State law also incorporates mandatory action into its episode avoidance plan for days when 

where air pollution levels are forecast.587. Such mandatory actions are included in permits for 

industry that specify actions to be taken at each alert level.588 The San Joaquin Valley Air 

Pollution Control District, which serves one of the most-ozone polluted areas in the nation, also 

incorporates similar action levels, triggered by the forecasted air quality, that puts enforceable 

requirements on permitted, stationary sources of ozone precursors.589 

With these and similar requirements and permits in place, the AQI often used by these 

systems to trigger behavior change begins at the Unhealthy (red) breakpoint, not the Unhealthy 

for Sensitive Groups (orange) breakpoint that usually corresponds to the level of the NAAQS. 

Therefore, it is critical that the level of Unhealthy be set in the AQI to ensure that it recognizes 

the higher risk at that level. 

The final AQI levels needs to provide adequate recognition of the higher levels of risk at 

the Unhealthy level. Under the proposal, EPA has provided a range of levels for the theshold into 

the unhealthy for sensitive groups category, based on the proposed standard. Unfortunately, the 

proposed AQI Breakpoints590 incorporate too great a range of ozone concentration into the 

Unhealthy for Sensitive Groups classification, pushing the threshold for the Unhealthy level far 

above where the actions they trigger should begin. 

Instead of having the threshold for Unhealthy begin at 85 ppb, we urge EPA to adopt a 

much lower threshold that would trigger these pollution reduction mechanisms that states and 

local agencies have been using to prevent the release of ozone precursors. Setting the breakpoint 

for Unhealthy at 85 ppb would, by EPA’s own rationale, not require the triggering of these 

pollution reduction measures until the air quality threatened to impact 25 percent of exposed 

people.591 However, the exposed people in the discussion in McDonnell et al, 2012, that EPA 

cites,592 are healthy adults and as we discuss elsewhere the burden of ozone harems the health of 

many people are far lower thresholds than the thresholds for healthy adults. Since McDonnell et 

al. state that this threshold should be shifted to recognize the impact on different populations, the 

AQI should also have the threshold shifted to recognize harm to the diverse population. 

 

586 http://air.utah.gov/forecastLegend.html

587 State of Washington. RCW 70.94.715. Air pollution episodes — Episode avoidance plan — Contents — Source 

emission reduction plans — Authority — Considered orders.

588 For example, see the Air Operating Permit from the Puget Sound Air Pollution Control Agency for the U.S. Oil 

and Refining Company, issued December 11, 2011. Accessed at 

http://wwwdev.pscleanair.org/library/Air%20Operating%20Permits%20Library/12593-faop.pdf on March 16, 

2015.

589 San Joaquin Air Pollution Control District. Current District Rules and Regulations. Regulation VI: Air Pollution 

Emergency Contingency Plan. Accessed at http://www.valleyair.org/rules/1ruleslist.htm on March 16, 2015

590 Proposed Rule at 75,311

591 Id.

592 Id.; McDonnell WF, Stewart PA, Smith MV, Kim CS, and Schelegle ES. Prediction for lung function response 

for populations exposed to a wide range of ozone conditions. Inhal Tox 20101; 24(10) 619-633.
220

For these reasons—the important role that the Unhealthily Category plays in efforts to 

reduce ozone precursors, and the need to recognize that the threshold needs to be shifted to 

accommodate the more sensitive populations—EPA should reconsider its AQI Breakpoints and

select a much lower threshold than 85 ppb as the breakpoint of for Unhealthy Category. 

2. Failing to Set the NAAQS At the Health Protective Level of 60 ppb 

Would Lead to the Dissemination of False Information and Rob 

People of Their Ability to Protect Themselves and Their Children 

From Unsafe Air.

The purpose of the AQI, the extent of its infrastructure, and the high degree of reliance 

exhibited by the public require that the NAAQS be set at a truly health protective level of no 

higher than 60 ppb. Setting the NAAQS any higher than 60 ppb will have the direct effect of 

depriving the public of knowing what health impacts they and their children might suffer on any 

given day, as the information conveyed to them will not accurately reflect the degree to which

the air in their surroundings presents a health risk. Consequently, it will also prevent the public 

from engaging in averting behavior (to the extent that doing so is possible) and thereby 

exercising their right to protect themselves and their children from the health effects of polluted 

air. Failing to set the ozone NAAQS at 60 ppb will therefore result in a perversion of the purpose 

of the AQI and the waste of its attendant infrastructure. 

The need for an accurate and reliable AQI is further underscored by the fact that episodes 

of unsafe air will occur even if the current round of ozone NAAQS revisions results in the setting 

of a health protective standard. First, because areas will (and are allowed to) take years to come 

into compliance with existing standards, unsafe air will continue to plague residents of those 

areas long after any new standards are issued.593 Further, because the current (and proposed) 

ozone NAAQS use the annual 4th-highest daily maximum 8-hour concentration averaged over 3 

years as the form of the standard, even areas that are in attainment of the (current or revised) 

standard will see numerous 8-hour periods (and are likely to see many more shorter periods) that 

exceed the standard in any given year. People living in such areas have the right to know whether 

and when the air they breathe is safe. Setting the NAAQS at the health protective level of 60 ppb 

is the only way to ensure that people living in these and all other areas have the information they 

need to protect themselves and their children. 

H. Appendix U: EPA’s Proposed Changes to Implementation Rules Would 

Undermine the Health and Welfare-Protectiveness of the Revised Standard 

and Are Inconsistent with the Act and its Regulations

1. The Language of the NAAQS Should Not Be Limited to Monitoring 

Sites; The Language Needs to Be Broad Enough to Take into Account 

the Potential Use of Modeling for Evaluating Attainment, Which 

Should Utilize a Full Receptor Grid Reflecting the Fact the NAAQS 

Are National Ambient Air Quality Standards

 

593 Air quality in 10% of the original 113 areas designated as non-attainment for the 1997 Ozone NAAQS still does 

not meet the 1997 standards and as of 46 areas were failing to attain the 2008 standards as of 2012. Proposed Rule at 

75,370.
221

EPA’s proposed language in the NAAQS itself, that is 40 C.F.R. § 50.19, is problematic. 

Specially, the references to reference and equivalent methods and monitoring sites in 40 C.F.R. 

§ 50.19(a), (b), (c), and (d) should be removed. Then, an additional subsection (e) should be 

added which says something to the effect of, “When a monitor is used to determine compliance 

with a NAAQS, it must be a reference method based on appendix D to this part and designated in 

accordance with part 53 of this chapter or an equivalent method designated in accordance with 

part 53 of this chapter.” 

EPA should make this change for three reasons. The first is that the proposed language 

invites challenges from polluters to the use of methods other than air monitors in determining 

compliance with the NAAQS. For example, polluters used a similar argument in trying to 

challenge the 2010 sulfur dioxide NAAQS and its implementation.

The second is that such language is used to justify modeling only at model receptors 

which are representative of ambient monitor locations. Such a modeling approach is illegal and 

not adequately protective of public health and welfare. Rather, in modeling, a full receptor grid 

should be used because this is a “national” standard. 

The D.C. Circuit has recognized the geographic limitations of monitoring. See e.g.

Catawba County v. EPA, 571 F.3d 20, 30 (D.C. Cir. 2009) (“EPA's selection of the county as the 

unit of analysis resolved a problem inherent in the monitoring process, namely, that a monitor 

only measures air quality in its immediate vicinity.”). There is no rational reason to export the 

inherent problem in monitoring into the modeling process. However, the proposed language of 

40 C.F.R. § 50.19(a), (b), (c), and (d) invites arguments for such an ill-conceived approach to 

modeling. 

Modeling only at receptors representing ambient monitor locations also violates the plain 

language of the statute and regulations. In National Ass’n of MFRS v. EPA, 750 F.3d 921, 926 

(D.C. Cir. 2014) the D.C. Circuit explained: “The point of the NAAQS program is to safeguard 

the quality of the "ambient air," which is defined as the "portion of the atmosphere, external to 

buildings, to which the general public has access." 42 U.S.C. § 7409(a); 40 C.F.R. § 50.1(e)”. It 

is contrary to the definition of ambient air to redefine ambient air as only the air at monitoring 

sites. EPA therefore, should take out references to air monitors in 40 C.F.R. § 50.19(a), (b), (c), 

and (d).

The third reason is EPA is proposing to use this language to weaken public health and 

welfare protection even further, and move further away from what the science says is the 

necessary level of protection, by not calculating design values for each monitor but rather for 

each site.594 This issue is discussed in detail below. 

2. Data Completeness: EPA Needs to Create a Methodology that Fills in 

Missing Data, Similar to 40 C.F.R. Part 75 of the Acid Rain Program

 

594 Proposed Rule at 75,351. 
222

EPA needs to create a methodology that fills in missing data, similar to 40 C.F.R. § Part 

75 of the Acid Rain program. Without this, the NAAQS cannot ensure the protection that EPA 

says it is choosing to provide. 

The metro-Atlanta ozone nonattainment area, for example, has missing data. Numerous 

times, hourly ozone levels trend significantly upward so that it looks almost certain that there 

will be an 8-hour average, but then the monitor becomes “unavailable” for some reason before 

enough data is gathered to get a violating 8-hour average.595 Currently, states do not have an 

external incentive to ensure they gather complete ambient monitoring data. EPA needs to create 

incentives and consequences for states having complete monitoring data. 

The current and proposed form and averaging time do not make adjustments for missing 

data. However, the old one-hour average did. While there is a minimum number of days that 

monitoring sites are required to collect, there is no consequence if the monitoring site fails to 

meet this standard. In any event, because the minimum standard is not 100% of the required 

days or hours, people can be and are exposed to significantly more short term periods about the 

level that EPA says is the appropriate level. EPA should add a data filling mechanism based on 

protective assumptions.

3. EPA Should Not Decrease the Number of Monitors Used to Calculate 

Design Values 

EPA is proposing to no longer consider design values from monitors other than the 

primary monitor that are located at multi-monitor sites.596 Not considering design values from 

monitors at multi-monitor sites is the same as reducing the number of monitors. EPA presents 

no reason why the number of monitors should be decreased while the standard is being made 

more protective, nor is there one. Rather, it is arbitrary to ignore data for monitors other than the 

primary monitor which EPA has in making regulatory decisions. 

EPA seems to imply that there is consistency across monitors at the same site. That is not 

always true. For example, AQS reports the 4th high for 2013 for monitor 1 at site 060430003 in 

Yosemite National Park at 0.073 ppm, or above the proposed NAAQS.597 However, AQS 

reports the 4th high for 2013 for monitor 2 at that same site as 0.056 ppm or below the proposed 

NAAQS.598 This is a 30 percent spread which could not be fairly described as consistent. Nor is 

this an isolated example. 

We do applaud EPA’s desire to make sure there are more complete sets of ambient 

monitoring data. However, as we explained in section V.H.2, the appropriate way to address this 

is to create a protocol for filling in missing data similar to the one used in the Acid Rain 

Program. 

 

595 Data available at http://www.air.dnr.state.ga.us/amp/ and incorporated herein by reference.

596 See Proposed Rule at 75,351.

597 See Exhibit 17 at 27. 

598 Id.
223

4. Data Handling: EPA Should Take an Approach that Is Rational, 

Protective and Consistent with the Statute

EPA’s current and proposed data handling conventions weaken the NAAQS by 

increasing the risk that people will actually be exposed to ozone levels above the levels EPA 

deems appropriate. We recommend EPA take another approach. Consistent with the 

Congressional intent that the Clean Air Act use a precautionary approach when it comes to 

exposing innocent people to toxic air pollution, EPA should use data handling conventions that 

err on the side of protecting people and the public welfare rather than ones that arbitrarily assume 

certain amounts of ambient ozone does not exist when we in fact know that it does. Below we 

discuss elements of the data handling convention and how EPA can implement them consistent 

with this guiding principle. 

EPA’s proposed data handling convention would require that any decimal digits reported 

beyond three decimal digits will be truncated.599 EPA’s stated reasons for this are (1) consistency 

with past practice and (2) typical measurement uncertainty.600

EPA must, at a minimum round the third decimal place rather than truncate. Past 

practices do not provide a rational basis to truncate in this context because monitoring equipment 

has changed over the decades since EPA started truncating. As to measurement uncertainty, 

truncating and rounding both address this uncertainty. However, rounding is more consistent 

with Congress’ clearly expressed will that NAAQS be addressed in a precautionary manner. See

42 U.S.C. § 7409(b)(1)(“allowing an adequate margin of safety”). Whatever convention EPA 

uses, that method must be accounted for in setting the level of the standard. As shown in part 

V.B.3.b.ii above, the use of such conventions can result in the standard being insufficiently

protective to prevent adverse effects.

Similarly, EPA should not substitute zero for one-half of the minimum detection level 

(MDL) as it is proposing in calculating 8-hour averages from the hourly ozone data when fewer 

than six hourly ozone concentrations are available during an 8-hour period.601 Substituting zero 

is arbitrary because there is no reason to believe the value is actually zero. Rather, a review of 

AQS shows hours with zero ozone levels are extremely rare. 

The most rational approach is to extrapolate the most reasonable approximation of the 

hourly value based on trajectory of the hourly values closest in time to the missing hourly value 

or some other mathematically acceptable way to approximate. This approach is also more 

consistent with Congress’ intent for a precautionary implementation of the NAAQS. This 

approach also moves the actual implementation of the standard closer to providing the protection 

against exposures of concerns which EPA claims to the public and CASAC that EPA is 

providing. Moreover, this need not be complicated, time consuming or resource intensive. It 

can be done using automated computer programs. 

 

599 Proposed Rule at 75,352. 

600 Id. 

601 Id. 75,352. 
224

EPA cannot lawfully or rationally get rid of the rule that provides for 8-hour daily 

maximums to include overlapping hours from two days.602 Again, EPA’s proposal moves the 

standard away from the protection EPA is claiming, especially since the human controlled 

exposure studies are often based on 6.6 hours of exposures not 8 hours so the exposure of 

concern is really shorter than the NAAQS form. In addition, this is not double counting from an 

individual exposures point of view. People come and go from areas. Moreover, EPA’s claim 

that post-sunset ozone peaks should not be counted because they “are assumed to be caused by 

transport of O3 molecules”

603 is doubly irrational. First, it’s based expressly on an unexplained 

assumption. Second, wherever the ozone came from, it’s present in the area and available for 

people to breathe. EPA must provide people the protection the Clean Air Act guarantees. 

Overall, using only the daily maximum is not supported by the controlled human exposure 

studies or by EPA’s regulatory stability argument. EPA shouldn’t make the problem of using 

only the daily maximum worse by its new proposal of only 17 8-hour periods in a day rather than 

24. 

EPA also proposes that there must be 13 of 17 8-hour periods in a day in order to 

determine a valid daily maximum.604 EPA says that it is including this requirement because 

13/17 is consistent with the 75% data completion requirement used for daily and annual 

NAAQS-related statistics.605 However, EPA proposes to keep the provision in 40 C.F.R. § 50, 

Appendix P which says that a daily maximum 8-hour average is valid if it is greater than the 

NAAQS. Id. The Appendix P language is mandatory: “a day shall be also be counted as valid”. 

40 C.F.R. § 50, Appendix P 2.1. The preamble used an unclear term “allowing.”606 We believe 

that the preamble was just lacking in precision and that the language in Appendix P 2.1 will 

remain mandatory. We support and believe the Clean Air Act mandates that any day with an 8-

hour average above the level of the NAAQS must be included in calculating the design value. 

5. Changes to Length of Monitoring Seasons

a. The Length of the Ozone Season Should be a Uniform 12 

Months

Over five years in the making, EPA is proposing to expand the length of the required 

ozone monitoring seasons in a number of states.607 We strongly support expanding the length of 

the ozone monitoring seasons. As further detailed below, ozone exceedances are recorded 

outside of the traditional ozone season in a number of states, and would likely be recorded in 

other states if the monitoring season was expanded. 

EPA’s proposal, however, does not go far enough. EPA is trying to set the ozone season 

to monitor when conditions are conducive to ozone formation.608 EPA tries to do this by looking 

at data from monitors which were operated outside of their ozone season. But, this approach 

 

602 Id.

603 Id. at 75,352-53

604 Id. at 75,353. 

605 Id. 

606 Id. 

607 Id. at 75,358. 

608 Id. 
225

almost certainly misses many situations in which ozone exceedances occur outside the traditional 

ozone season because approximately 700 monitors do not operate year round.609 In addition, 

EPA’s current methods for determining what conditions are conducive to ozone formation are 

overly conservative. For example, EPA used to believe that ozone was not formed in the winter 

time in colder climates. However, the designation of part of southwest Wyoming as 

nonattainment for the 2008 ozone NAAQS demonstrates the error of that belief.610 Climate 

change is also likely to increase the length and severity of ozone seasons. To assure more 

complete identification of the periods in which ozone exceedances occur, EPA needs to require 

all monitors to operate year round. 

Furthermore, EPA’s use of only one year of data in some instances to determine if they 

ozone season needs to be extended arbitrarily excludes situations in which looking at more than 

one year would show the need for such extended monitoring. See 79 Fed. Reg. at 75,358. 

The fact that EPA’s proposed increase in ozone seasons would only cost $230,000611 is a 

strong indication that increasing all ozone monitors to year-round would also cost a modelst 

amount. Furthermore, the Clean Air Act requires that this cost be covered by permit fees, not by 

state agencies’ general budgets. The cost of increasing all monitors to year round monitoring 

would be truly trivial when spread across all permitted polluters.

In addition, the regulations cannot allow the Regional Administrators to change the 

regulations regarding ozone season without notice and comment. This would be an APA and/or 

CAA violation. It also would be very misleading for the public who often rely on the ozone 

monitoring data which is communicated to the public to make decisions to protect the health and 

lives of their families. If an ozone season is changed without public notice, people may assume 

that ozone levels are safe when in fact they are not safe but there is no monitoring being 

conducted to report ozone levels to the public. Note, however, that we do fully support 

revocation of previous Regional Administrator-granted waiver approvals. 

Also, EPA proposes not to increase the PAMS monitoring season from the current 3-

month June-August period.612 EPA does so even though it acknowledges that “in many areas the 

highest O3 concentrations are observed outside of the PAMS season.” Id. CASAC recommended 

extending the season and making it more flexible.613 Countering those considerations, EPA 

points only to “the potential burden associated with a lengthening of the PAMS season” and the 

value of a uniform season to “provide a consistent data set.”614 That is not a rational explanation 

for refusing to gather more, better data.

b. Barring Year-Round Monitoring in All Areas, EPA Should 

Ensure that States Where There Is or May Be Winter-Time 

 

609 Id. at ftnt. 232. 

610 In addition, states sometimes claim that their ozone problems are caused by long range transport of ozone, 

including international transport. To the extent this is true, an ozone season based on local conditions would be 

arbitrary because it fails to consider conditions where the ozone is allegedly created. 

611 Proposed Rule at 75,360

612 Id. at 75,365.

613 Id.

614 Id.
226

Ozone Season Problems Including All of the Region 8, 9 and 10 

States, Should Have Year Round Ozone Monitoring

Even if EPA were to reject our recommendation to increase the ozone monitoring season 

to 12 months for all monitors, EPA still needs to make changes to its proposed ozone monitoring 

seasons. EPA claims that places like Montana and South Dakota only have 4 month long ozone 

seasons. This is inconsistent with winter time ozone monitoring data when it was actually done 

in the winter for similar places like Wyoming as evidenced by the fact that SW Wyoming is now 

a designated nonattainment area. In fact, EPA plainly states: “As an example, the highest O3 

concentrations in the Mountain-West often occur during the winter months.”615

Yet for the Mountain-West state of Wyoming, EPA’s proposal is to not require 

monitoring during the winter months of October, November and December.616 While it is true 

that winter technically begins on December 21st, it is common knowledge that Wyoming 

experiences what anyone would describe as winter weather during the months of October, 

November and December. For example, in Rock Springs, Wyoming, the average high and 

average low temperature in December is the same as in January.617 The average snowfall in 

December is just one inch different than the average snowfall in January.618 Thus, it is arbitrary 

to not require ozone monitoring in December but require it in January when the ozone formation 

factors are very similar. October and November, while slightly warmer on average, also have 

almost the same snowfall average as January, February and March. Since snowfall is probably 

an important factor in wintertime ozone formation, it makes sense to also require ozone 

monitoring in October and November. 

Montana, South Dakota and North Dakota are in a similar situation to Wyoming. The 

Bakken oil patch has resulted in an exponential increase in ozone precursor emissions in this 

area. Montana is actually in the “Mountain-West” which EPA says often experiences its highest 

ozone concentrations in winter months.619 Yet, contrary to its own admitted fact, EPA is not 

proposing to require ozone monitoring Montana during winter months.620 

It is not clear whether EPA believes the Mountain-West to include South Dakota and 

North Dakota. It is clear that the Bakken oil patch is mainly in North Dakota and its ozone 

precursor emissions are skyrocketing. In 2013, the most recent year of undisputedly final ozone 

data, all 9 of North Dakota’s ozone monitoring sites experienced 8-hour ozone values of 0.060 

ppm or greater according to EPA’s AQS. Although slightly colder, Watford City, North Dakota, 

for example, gets similar amounts of wintertime precipitation and snow as Wyoming.621 Thus, 

EPA should create a year round ozone monitoring season for Wyoming, Montana, North Dakota 

and South Dakota. 

6. Changes to Monitoring Network 

 

615 Id. at 75,365. 

616 Id. at 75,410. 

617 See Exhibit 19.

618 Id. 

619 Id. at 75,365. 

620 Id. at 75,410. 

621 See Exhibit 19 and Exhibit 20. 
227

The current ozone monitoring network is inadequate. One example of this is the recent 

discovery that the Upper Green River Basin area in Wyoming is violating the 2008 ozone 

NAAQS. Another example is Metropolitan Statistical Area (MSAs) are not required to have 

monitors and 105 of these MSAs, with a combined population of 18 million people, did not have 

monitors that gathered enough data to determine a design value.622 EPA has concluded that there 

is a reasonable likelihood that many of these MSAs would have violated the 2008 NAAQS.623 

Moreover, the monitoring network is inherently inadequate because monitors only measure air 

quality in their immediate vicinity. Catawba County v. EPA, 571 F.3d at 30. EPA 

acknowledged the inadequacy of the monitoring network before by proposing to modify the 

minimum monitoring requirements in urban areas and adding new minimum monitoring 

requirements in non-urban areas. 74 Fed. Reg. 34,525 (July 16, 2009). Unfortunately, EPA 

never finalized the 2009 Proposal. EPA should use this rulemaking as an opportunity to begin to 

address this problem.

First, consistent with the 2009 Proposal, EPA should modify the minimum ozone 

monitoring requirements to require at least one monitor to be placed in MSAs of populations

ranging from 50,000 to less than 350,000. This would help ensure that an additional 18 million 

people or more are not being exposed to dangerous or deadly ozone pollution.624 

Second, to ensure protection consistent with both the secondary and primary NAAQS, 

and again consistent with the 2009 Proposal, EPA should require states to have ozone monitors 

in three categories of non-urban areas. The first required non-urban monitor should be located in 

areas such as some federal, state, or tribal lands, including wilderness areas that have ozonesensitive natural vegetation and/or ecosystems. Exhibit 21 lists ozone -sensitive natural 

vegetation.625 

The second required non-urban monitor category should be required to be placed in a 

MSA expected to have ozone design value concentrations of at least 85 percent of the NAAQS. 

This is important because EPA’s rules should not discriminate against people who live in rural 

areas. In addition, many MSAs may have low residential numbers and yet are tourist areas 

where many more people spent time engaged in outdoor physical activity which EPA has 

repeatedly acknowledges makes them more at risk of injury ozone population. For example, 

evidence indicates that the elevated ozone levels in the front range of Colorado extend all the 

way up to the continental divide.

626

 Yet, there are no regulatory monitors in Western Boulder 

County, Gilpin, Clear Creek, Summit, Park, Teller, Fremont, Custer, and Huerfano Counties and 

thus none of the front range mountain counties are designated non-attainment except Boulder 

County based on urban monitors. While these counties have relatively low residential 

populations, millions of people engage in outdoor activities in these counties. These areas 

 

622 74 Fed. Reg. 34,525, 34,527 (July 16, 2009)(2009 Proposal). 

623 Id. at 34,528.

624 To the extent EPA is concerned about a procedural challenge to such a requirement, EPA could finalize the 2009 

proposal in the same rule that finalized the ozone NAAQS. 

625 See Exhibit 21 at 11-13. 

626 See e.g. Exhibit 18. Note that the NCAR Frappe study and NASA Discovery AQ studies, to which this article 

refers have not released all of their data to the public yet. However, EPA is participating in the NCAR Frappe study. 

Thus, all data from this study currently in EPA’s files are incorporated herein by reference. 
228

include ski areas which host year round activities as well as wilderness areas and national and 

state parks. Many of the activities engaged in these areas such as hiking, backpacking, mountain 

biking, and skiing are very physically demanding resulting in increased respiration. Even 

moderate exercise or no exercise in these communities can result in significant increases in 

respiration for people not used to the elevation, thus increasing their ozone exposure. Yet the 

current monitoring network design completely fails to address this situation. Similar situations 

can be found in other Western states. 

The third required non-urban monitor should be in the area of expected maximum ozone 

concentration outside of any MSA, potentially including the far downwind transport zones of 

currently well-monitored urban areas. This expectation should consider any creditable evidence 

of potential high ozone levels. This includes monitors that are not formally a part of EPA’s 

regulatory system as well as credible data from computer models, satellites and aircraft 

measuring ozone. 

7. Implementation Issues 

a. Prevention of Significant Deterioration: Significant Emission 

Rates and Significant Impact Levels

In the Proposal, EPA briefly discusses various screening tools used to assess whether or 

not a source must undertake Prevention of Significant Deterioration (PSD) review. The agency 

notes that it has established a “Significant Emission Rate” (SER) for ozone precursors (VOCs 

and NOx) of 40 tons per year (tpy), and that the agency uses 100 tons per year as a substitute of 

sorts for a Significant Impact Level (SIL), which it has not yet set for ozone.

627 The agency 

further notes that it “intends to consider whether it is appropriate to make any revisions to the 

PSD regulations related to the screening tools for [ozone] in a separate rulemaking...”628 It is of 

critical importance that EPA undertake revisions to the SER and SIL-like tools (though not 

create a SIL). Although we applaud the agency for planning to undertake the analysis required to 

revise these tools, we believe that these revisions should be undertaken contemporaneously with 

this and any other update to NAAQS.

i. Significant Emission Rates

A Significant Emission Rate set at 40 tpy is entirely inappropriate in the context of the 

proposed rulemaking. A SER set at 40 tpy for NOx and VOCs has no rational relationship to a 

revised 8-hour ozone standard. SERs are used to determine “where pollutant emissions or 

ambient impacts could be considered de minimis,” and there is nothing to suggest that 40 tons 

per year is a de minimis level of pollution under any revised standard.

629

EPA claims authority to set de minimis exceptions to NSR permitting based on from 

Alabama Power v. Costle. 636 F.2d 323 (D.C. Cir. 1979). In that case, the D.C. Circuit suggested 

that EPA could exempt from PSD review some emission increases on de minimis grounds. 636 

 

627 Proposed Rule at 75,379.

628 Id.

629 Id.
229

F.2d at 400. As the Court made clear, however, the burden of justifying any such exemption 

would be on EPA, and the agency’s inquiry must focus on the statutory goals: 

Unless Congress has been extraordinarily rigid, there is likely a basis for an 

implication of de minimis authority to provide exemption when the burdens of 

regulation yield a gain of trivial or no value. That implied authority is not 

available for a situation where the regulatory function does provide benefits, in 

the sense of furthering the regulatory objectives, but the agency concludes that 

the acknowledged benefits are exceeded by the costs. 

Id. 360-61 (emphasis added).

When implementing Alabama Power, EPA acknowledged that it could not label any 

pollution levels “de minimis” unless it first determined “the cumulative effect on increment 

consumption of multiple sources in an area each making the maximum de minimis emissions 

increase (thereby going unreviewed under PSD at the time of the change).”630 That is, the agency 

recognized (1) that the Clean Air Act proscribes increment violations; (2) that PSD is a vital 

mechanism for enforcing increment restrictions; and thus, (3) that the agency lacks authority to 

exempt de minimis pollution increases from PSD if there is any chance that such exemptions 

could, individually or cumulatively, lead to increment violations.

While one source may modify its facility and not cause a significant air quality 

impact, a number of sources making such a change could cause a significant 

impact. If the sources were located near to each other, the cumulative air quality 

impact could consume a significant amount of the increment. Since the extent of 

the impact is directly proportional to the number of sources and their relative 

proximity to each other, it is important to determine the potential air quality 

impact from a number of existing sources making de minimis changes in 

emissions.631

The same analysis must, logically, hold for NAAQS violations.

Fundamentally, the methodology utilized by EPA for determining NSR applicability 

must be consistent with the agency’s obligation to ensure that the PSD permitting program 

prevents modified sources from “caus[ing], or contribut[ing] to” an increment or NAAQS 

violation reflecting actual NAAQS in place as a matter of law. The last time the Agency 

apparently undertook such exercise was in 1980 when the ozone NAAQS was 120 ppb.632 The 

Agency has done nothing to show that the current SER of 40 tpy, as keyed to an updated 

standard, would ensure that such increment or NAAQS violations were prevented. 

As such, we urge EPA to move forward with revisions to its PSD screening tools as 

quickly as possible. We also ask that the Agency include in this rulemaking any information on 

 

630 45 Fed. Reg. 52,676, 52,707 (Aug. 7, 1980).

631 U.S. EPA (1980). Impact of Proposed and Alternative De Minimis Levels for Criteria Pollutants, 7 (EPA-450/2-

80-20).

632 45 Fed. Reg. 52,676, 52,732 (Aug. 7, 1080).
230

the sufficiency of a 40 tpy SER to prevent air quality violations relating to the range of standards 

proposed in the rulemaking. The SER cannot be disconnected from the level of the NAAQS as is 

the case with the levels set in 1980. 

Should EPA lower the NAAQS for ozone, it must provide a rational basis for concluding 

that the existing SER continues to be appropriate.

ii. Significant Impact Levels

EPA notes that SILs are used to “determine the extent to which an ambient impact 

analysis must be completed for the applicable pollutant,” and that the Agency has yet to set a SIL 

for ozone. 79 Fed. Reg. 75,379. We do not agree that SILs are lawful or rational for reasons 

given in comments on EPA’s PM2.5 increment rule, which we adopt by reference. EPA-HQOAR-2006-0605-0040. In the event that EPA persists with using SILs and SIL-like tools, we 

offer the following comments. 

Current regulations state that “any net emissions increase of 100 tons per year or more of 

[VOC] or [NOx] subject to PSD would be required to perform an ambient impact analysis, 

including the gathering of air quality data.” 40 CFR § 51.166(i)(5)(i). EPA goes on to note that 

these values 

do not reflect a categorical conclusion by the EPA that sources emitting less than 100 tpy

of VOCs or NOx will not cause or contribute to a violation of the current (or any revised) 

O3 NAAQS, nor does it reflect a conclusion that such sources should be categorically 

excluded from the requirement for an ambient impact analysis.

Id.

 The ambiguous and vague nature of this statement underscores that EPA must revise the 100 

tons/year threshold for ambient impact analysis found in 40 C.F.R. § 52.21(i)(5)(i) and 

51.166(i)(5)(i). There is no record in the docket for this rulemaking or elsewhere to demonstrate 

that NOx and VOC emission levels set at 100 tpy are de minimis in relation to any new ozone 

NAAQS, nor even, as the Agency itself notes, the current NAAQS. In a recent response to a 

petition for rulemaking on this issue, the Administrator noted that in the 1990 NSR Workshop 

Manual, at page C.28 footnote b, the Agency 

sa[id] the following with respect to the then-applicable one-hour ozone NAAQS: ‘No 

significant ambient impact concentration has been established. Instead, any net emissions 

increase of 100 tons per year of VOC subject to PSD would be required to perform an 

ambient impact analysis.’

The Administrator allowed that “based on these statements, this 100 [tpy] value has been used by 

some permitting authorities in a manner similar to a SIL to assess whether a detailed air quality 

analysis should be conducted for ozone.”633

 

633 Letter from Gina McCarthy, U.S. EPA Assistant Administrator, to Robert Ukeiley, at 4 (Jan. 4, 2012), available 

at http://www.epa.gov/scram001/10thmodconf/review_material/Sierra_Club_Petition_OAR-11-002-1093.pdf.
231

The Agency acknowledges in the same letter that the 100 tpy level has “not been 

revisited by the EPA since the promulgation of the 8-hour ozone NAAQS and do not reflect a 

categorical conclusion by the EPA that every source emitting less than 100 TPY of NOx or 

VOCs will not cause or contribute to a violation of the current ozone NAAQS.”634

The Agency itself has, in this rulemaking and others, allowed that the 100 tpy threshold 

functions “in a manner similar to a SIL” but at the same time asserts that “the EPA has not 

established a SIL for O3.”635 As noted above, the court in Alabama Power made clear that the 

Agency’s discretion does not extend beyond the confines of the statutory language. For reasons 

stated in the briefs for Sierra Club in Sierra Club v. EPA, 705 F.3d 458 (D.C. Cir. 2013) 

(incorporated by reference), we contend that the Clean Air Act forecloses the use of SILs to 

avoid or truncate the demonstration required by 42 U.S.C. §7475(a)(3). Accordingly, EPA needs 

to make clear that sources must undertake an individualized and comprehensive analysis in 

consultation with the appropriate EPA regional office to ensure that pollutant emissions and 

ambient impacts from the source are fully evaluated and considered, and demonstrate that the 

source's emissions will not cause or contribute to a violation of the NAAQS.

b. SIP requirements, Schedules and Attainment Dates

In setting a schedule to implement updated NAAQS, the Clean Air Act’s statutory 

language itself provides the requirements that states must meet in preparing state implementation 

plans to attain and maintain compliance with the updated ozone standards. The deadlines the Act 

establishes are outer time limits, however: nothing prevents EPA from encouraging states to 

coordinate their submissions of SIP elements by submitting some of them earlier than the last 

possible day. For the purposes of the rulemaking at issue here, nothing prevents EPA from 

issuing schedules for states contemporaneously with the issuance of an updated NAAQS, to 

facilitate states’ timely submissions. We urge EPA to take that approach here, as it ensures 

timely achievement of the goals laid out in the Act, and assists the states in ensuring that their 

recommendations to EPA are as well-informed by appropriate information and methodologies as 

possible.

Specifically, EPA notes that it intends to propose guidance or rules for “assisting with 

implementing any revised O3 NAAQS resulting from this proposal within 1 year after a revised 

NAAQS is established.”636 In particular, EPA notes that it is considering rules relating to 

“nonattainment area classification methodologies, SIP due dates, attainment dates, and required 

implementation programs such as NNSR and conformity.”637 The agency estimates that the rules 

will be finalized 2 years after the NAAQS issue.638

To the extent EPA intends to issue such rules we urge EPA to issue SIP requirements, 

schedules, and attainment dates as quickly as possible, and strongly suggest that the agency 

 

634 Id.

635 Cf. McCarthy Letter at 4, 79 Fed. Reg. 75,379.

636 Proposed Rule at 75,373.

637 Id. 

638 Id. at 75,374.
232

consider finalizing these requirements contemporaneously with any updated NAAQS. However, 

compliance with statutory time frames for implementing the NAAQS is not contingent on 

issuance of EPA rules, and any delay in issuance of such rules will not in any way excuse such 

compliance.

c. EPA Has No Authority to “Grandfather” Sources Out of PSD 

Requirements 

EPA proposes to amend the federal PSD permitting regulations in 40 C.F.R. § 52.21 to 

allow certain PSD permit applicants to avoid demonstrating that their project will not cause or 

contribute to violations of a new ozone NAAQS.

639

 The plain and unambiguous language of 

Clean Air Act section 165, however, does not confer on EPA any authority to exempt, or 

“grandfather” permit applicants from the statute’s PSD permitting requirements.640

EPA admits to no ambiguity in the requirements of the statute. Section 165(a) provides: 

No major emitting facility on which construction is commenced after August 7, 1977, 

may be constructed in any area to which this part applies unless—

... 

(3) the owner or operator of such facility demonstrates, as required pursuant to section 

7410(j) of this title, that emissions from construction or operation of such facility will not 

cause, or contribute to, air pollution in excess of any 

(A) maximum allowable increase or maximum allowable concentration for any 

pollutant in any area to which this part applies more than one time per year, 

(B) national ambient air quality standard in any air quality control region, or 

(C) any other applicable emission standard or standard of performance under this 

chapter.

42 U.S.C. § 7475(a). The plain language of section 165 defines the applicability of these 

provisions based on when construction commences, not on any stage of the permit application 

process. Id. (imposing requirements on facilities “on which construction is commenced after 

August 7, 1977”). EPA acknowledges that it interprets the language of the CAA “to require that

PSD permit applications must include a demonstration that new major modifications will not 

cause or contribute to a violation of any NAAQS that is in effect as of the date the PSD permit is 

issued.”641 The only major emitting facilities that are exempted by this plain language are those 

for which construction commenced by August 7, 1977. Id. § 7475(a); see also id. § 7478(b). 

This plain meaning is reinforced by the purposes of the PSD program, the statutory structure 

around the program, and the legislative history behind it.

The express purposes of the PSD program include: 

 

639 Id. at 75378 and 75404 (proposing amendments to 40 C.F.R. § 52.21(i)(12))

640 To the extent EPA intends to issue such rules, because of this potentially compressed timetable, we urge EPA to 

issue SIP requirements, schedules, and attainment dates as quickly as possible, and strongly suggest that the agency 

consider finalizing these requirements contemporaneously with any updated NAAQS. However, compliance with 

statutory time frames for implementing the NAAQS is not contingent on issuance of EPA rules, and any delay in 

issuance of such rules will not in any way excuse such compliance.

641 Proposed Rule at 75,377.
233

(1) to protect health and welfare from any actual or potential adverse effect which may be 

reasonably anticipate[d] to occur from air pollution...notwithstanding attainment and 

maintenance of all national ambient air quality standards; 

(2) to preserve, protect, and enhance air quality in national parks...and other areas of 

special...value; 

(3) to ensure that economic growth will occur in a manner consistent with the 

preservation of existing clean air resources; [and] 

. . .

(5) to assure that any decision to permit increased air pollution...is made only after 

careful evaluation of all the consequences of such a decision and after adequate 

procedural opportunities for informed public participation in the decision-making 

process.

42 U.S.C. § 7470. EPA’s proposal – which would allow projects to be built without a 

demonstration that they will not cause or contribute to a violation of the new ozone standards, 

which are being promulgated specifically to protect public health and welfare – cannot be 

reconciled with any of these stated purposes. “Grandfathering” projects does not protect public 

health, preserve air quality, or ensure economic growth is consistent with the preservation of air 

resources, and precludes careful decision-making and informed public participation.

When EPA adopted regulations implementing the PSD program in 1980, the Agency 

expressly rejected similar requests for “grandfather” exemptions based on these same clearly 

stated statutory purposes.642 Specifically, in its final rule, EPA rejected a commenter’s 

suggestion that EPA “promulgate a grandfather provision that would use the date of complete

application instead of the date of permit issuance” in determining the applicability of section 

165’s requirements.643 As the Agency noted, the “[u]se of such date, however, might exempt 

more projects from review” and “fail to give adequate expression to the interests behind section 

165, especially the goal of protecting air quality.” Id. 

When Congress adopted the PSD permitting program, it understood that certain sources 

might be affected by changing permit requirements. See H.R. Rep. No. 95-294, 95th Cong., 1st 

Sess., at 171 (1977) (“Safeguards against moratorium growth”). Consequently, Congress limited 

the applicability of these new requirements in several ways, such as exempting existing sources 

and requiring only “major sources of air pollution” to obtain PSD permits. Id.; see 42 U.S.C. § 

7475(a). Congress also provided specific “grandfathering” relief to sources on which 

“construction had commenced” before the enactment of the 1977 Clean Air Act Amendments. 

See 42 U.S.C. § 7478(b) (“In the case of a facility on which construction was commenced...after 

June 1, 1975, and prior to August 7, 1977, the review and permitting of such facility shall be in 

accordance with the regulations for the prevention of significant deterioration in effect prior to 

August 7, 1977.”). Where, as here, Congress has provided express exemptions and not others, 

EPA is not free to invent new authority to waive otherwise applicable statutory requirements. See 

Andrus v. Glover Constr. Co., 446 U.S. 608, 616-17 (1980) (“Where Congress explicitly 

enumerates certain exceptions to a general prohibition, additional exceptions are not to be 

 

642 45 Fed. Reg. 52,676 (Aug. 7, 1980). 

643 Id. at 52,683. 
234

implied, in the absence of evidence of a contrary legislative intent.”). 

In enacting the PSD program, Congress also made the fundamental policy choices that 

(1) it is preferable to prevent air pollution from becoming a problem in the first place by limiting 

pollution created by newly constructed sources; and (2) controls should be installed when new 

sources are being constructed rather than as retrofits on existing sources. See S. Rep. No. 95-127, 

95th Cong., 1st Sess., at 11 (1977) (“This legislation defines ‘significant deterioration’ in all 

clean air areas as a specified amount of additional pollution.... This definition is intended to 

prevent any major decline in air quality currently existing in clean air areas and will provide a 

margin of safety for the future.”); H.R. Rep. No. 94-1175, 94th Cong., 2d Sess., at 101 (1976) 

(noting that “‘an ounce of prevention is worth a pound of cure’” and explaining that 

“[p]ermitting unrestricted deterioration of air quality up to ambient standards involves trying to 

cure a condition after it has developed rather than using practical and currently available means 

to prevent or minimize the condition in the first place”); id. at 108 (“Common sense dictates that 

it is substantially less expensive to prevent air pollution problems – and health problems – before 

they develop than it is to abate dangerous pollution levels.... This approach will allow us to avoid 

future massive air pollution concentrations which endanger public health and restrict further 

economic growth, require expensive retrofitting of pollution control technology and produce 

demands for economically and socially disruptive restrictions on the use of automobiles and on 

indirect sources.”). EPA’s proposal would actively defeat both of these policy choices.

EPA’s proposal would allow projects to be built without demonstrating that they will not 

cause or contribute to violations of the ozone standards. If these sources are built and it is 

subsequently determined that violations are occurring as a result of their emissions, the States 

will be responsible for developing plans to control emissions to meet the standards. 42 U.S.C. §§ 

7410, 7502. Such plans would require the adoption of reasonably available control technology 

requirements for existing major sources. 42 U.S.C. § 7502(c)(1). The result is that these same 

sources given a pass under the PSD program could be required to address these emissions in a 

much less cost-effective manner through retrofit controls. Grandfathering sources from section 

165’s requirements, and ignoring the foreseeable pollution problems that the PSD program is 

specifically designed to avoid, clearly undermines the “prevention” purpose of the PSD program 

and the policy choices made by Congress. 

The statutory language of Clean Air Act section 165(a) is plain – a new source must 

demonstrate that it will not cause or contribute to a violation of any national ambient air quality 

standards. Unless the source can meet these criteria, it may not be built. 

EPA does not suggest that there is ambiguity in the statutory language of section 

165(a)(3). Yet EPA maintains that it is nonetheless free to waive these requirements through 

rulemaking following the adoption of a new NAAQS.644 EPA suggests that such discretion 

derives from the fact that, under CAA section 165(c), the agency must grant or deny a permit 

within one year of a completeness determination, and its general rulemaking authority in CAA 

section 301.645 EPA’s arguments lack merit.

 

644 See 79 Fed. Reg. at 75377. 

645 See id. 
235

The initial premise of EPA’s argument is false. Even assuming the promulgation of a 

new NAAQS might lead to the inability to approve a permit within the deadlines of section 

165(c) – a conclusion that has no actual record basis – such inability does not create a conflict or 

tension with the requirements of section 165(a)(3). First there is no actual conflict between these 

sections. If EPA cannot approve the project within the applicable deadline while also finding 

that the source has met its statutory obligations regarding air quality protection, the appropriate 

resolution is either to deny the permit application because it does not meet the requirements of 

the statute, or to acknowledge that with the promulgation of a new NAAQS the application is no 

longer complete. 

Second, even if it turned out to be impossible to comply with both sections, that failure 

does not create a conflict that allows EPA to pick which section it is going to ignore. A 

fundamental canon of statutory construction is that “[a] statute should be construed so that effect 

is given to all its provisions, so that no part will be inoperative or superfluous, void or 

insignificant.” Hibbs v. Winn, 542 U.S. 88, 101 (2004) (internal quotation and citation omitted); 

see Bernier v. Bernier, 147 U.S. 242, 245 (1893) (“[I]t is a general rule, without exception, in 

construing statutes, that effect must be given to all their provisions, if such a construction is 

consistent with the general purposes of the act, and the provisions are not necessarily 

conflicting.”). As the Supreme Court recently explained, the agency’s “authority and 

responsibility to resolve some questions left open by Congress that arise during the law’s 

administration” does not extend to “include a power to revise clear statutory terms that turn out 

not to work in practice.” Utility Air Regulatory Grp. v. EPA, 134 S.Ct. 2427, 2446 (2014). “An 

agency confronting resource constraints may change its own conduct, but it cannot change the 

law.” Id.

EPA’s faulty line of reasoning has already been considered and refuted by the U.S. 

Supreme Court in General Motors Corp. v. United States, 496 U.S. 530 (1990). In General 

Motors, industry argued that EPA’s failure to act on a state implementation plan (SIP) revision 

within the statutory period for review under section 110 of the Act precluded EPA from 

enforcing the existing provisions of the SIP under section 113. Id. at 535. The Supreme Court 

rejected the contention that there was a conflict in the statute, holding that delay on the part of 

EPA does not affect the Agency’s ability to enforce the other requirements of the Act. Id. at 

539-42. In other words, a violation of one provision does not affect the applicability of other 

requirements unless the statute provides otherwise. General Motors, 496 U.S. at 540-42; see 

also United States v. James Daniel Good Real Property, 510 U.S. 43, 63 (1993) (“We have held 

that if a statute does not specify a consequence for noncompliance with statutory timing 

provisions, the federal courts will not in the ordinary course impose their own coercive 

sanction”).

Third, to the extent there is any real problem, it is a problem within EPA’s ability to 

manage. There is no reason that modeling cannot be conducted now by permit applicants, 

pending final promulgation of the ozone standard, that assesses compliance with an ozone 

standard down to 60 ppb. If a particular proposed project would cause or contribute to a 

violation of a lower standard it can prepare accordingly without delaying review of the permit.
236

With no ambiguity or gap in the statutory language, EPA has no ability allow sources to 

avoid the statutory mandates. Nothing in the statute gives EPA the power to waive the 

requirements of section 165(a), which are self-effectuating and directly enforceable against the 

source.

EPA suggests that it has general rulemaking authority in section 301 to alter these 

otherwise plain requirements. The courts, however, have repeatedly rejected such a notion. 

Section 301(a)(1) authorizes EPA to “prescribe such regulations as are necessary to carry out 

[its] functions under [the Act].” 42 U.S.C. § 7601(a)(1). The D.C. Circuit, however, has 

“consistently held that EPA's authority to issue ancillary regulations is not open-ended, 

particularly when there is statutory language on point.” NRDC v. EPA, 749 F.3d 1055, 1063 

(D.C. Cir. 2014); see also Am. Petroleum Inst. v. EPA, 52 F.3d 1113, 1119 (D.C. Cir.1995) (“the 

general grant of rulemaking power to EPA cannot trump specific portions of the CAA”); NRDC 

v. Reilly, 976 F.2d 36, 41 (D.C. Cir.1992) (rejecting EPA’s use of general rulemaking authority 

to add to a statutorily specified list); Sierra Club v. EPA, 719 F.2d 436, 453 (D.C.Cir.1983) 

(same). As the court explained: “Th[e]se precedents establish a simple and sensible rule: EPA 

cannot rely on its gap-filling authority to supplement the Clean Air Act's provisions when 

Congress has not left the agency a gap to fill.” NRDC, 749 F.3d at 1064.

EPA’s reliance on the fact that it has adopted similar illegal exemptions in the past also 

does not provide any authority to continue such practices here. See, e.g., New Jersey v. EPA, 517 

F.3d 574, 583 (D.C. Cir. 2008) (“[P]revious statutory violations cannot excuse the one now 

before the court.”); F.J. Vollmer Co. v. Magaw, 102 F.3d 591, 598 (D.C. Cir. 1996) (“[W]e do 

not see how merely applying an unreasonable statutory interpretation for several years can 

transform it into a reasonable interpretation.”). 

Nor does dicta from the Ninth Circuit’s Avenal decision support the notion that EPA has 

any authority to waive plain statutory requirements.646 The Ninth Circuit found the statute 

unambiguous on the question of whether section 165(a)(3) required sources to demonstrate 

compliance with the NAAQS in effect at the time of permit issuance. See Sierra Club, 762 F.3d 

at 981 (holding that permitting delay did not endow EPA with authority to waive NAAQS by 

rewriting unambiguous statutory terms). With no authority to change these unambiguous 

requirements, that is the end of the statutory analysis.

The Avenal court’s continued discussion of past grandfathering exemptions reflects a 

misunderstanding of EPA’s actions. The court seemed to believe that EPA had avoided 

imposing new NAAQS by adjusting the operative dates of those NAAQS. See id. at 983 (noting 

“[o]n almost every prior occasion, EPA grandfathered a limited set of applications, in effect, by 

specifying an operative date (or dates) for each new regulation, as it was formally adopted. In 

contrast to the ad hoc waiver here, the former procedure does not, on its face, violate the plain 

statutory mandate to enforce whatever regulations are in effect at the time the agency makes a 

final decision.”). As EPA is well aware, it is not proposing to “grandfather” sources by changing 

the operative date of the new ozone NAAQS. Instead it is waiving “the plain statutory mandate 

to enforce whatever [NAAQS] are in effect at the time the agency makes a final decision.” Id. 

As the Ninth Circuit found, EPA has no such statutory authority.

 

646 See Proposed Rule at 75,377 (citing Sierra Club v. EPA, 762 F.3d 971, 983 (9th Cir. 2014)).
237

 

The statutory language of Clean Air Act section 165(a) is plain – a new source must 

demonstrate that it will not cause or contribute to a violation of any national ambient air quality 

standards. Unless a source can meet these requirements, it may not be built. The statute 

provides no authority for EPA to waive these requirements, so the proposed grandfathering 

exemption should be dropped from the final rule.

d. Designations

EPA explains that it intends to issue guidance and rules that will help implement the 2015 

NAAQS in a timely manner.647 We applaud this goal. However, EPA’s track record on 

timeliness when it comes to implementing the Clean Air Act is not good. If EPA truly wants to 

take timely action, it seems like EPA would need to make fundamental changes in its processes 

in order to achieve this goal.

Specially, EPA claims that it will issue guidance for the designation process within 4 

months of promulgating the NAAQS.648 In order to do that, EPA should be working on that 

guidance now. 

As to designations for the secondary standard, if the standard is mainly driven by the 

protection of ecologically sensitive areas, EPA should include in its rationale for designations 

that same considerations. For example, if there is a violating monitor in a multi-county national 

park or wilderness area, EPA should include the entire national park or wilderness area in the 

nonattainment area. 

Furthermore, for the secondary standard EPA should use a more expansive definition of 

“nearby” when considering what areas contribute to ambient air quality in a nearby area that 

does not meet the secondary standard. In the context of intrastate pollution, it is critical that EPA 

designate areas that contain sources that contributing to nonattainment. For example, if a power 

plant in a rural area several counties over from a violating monitor in a national park is 

contributing to that violating monitor, EPA needs to designate the area around the power plant as 

nonattainment. Failure to do so will undermine the Act’s scheme for bringing the nonattaining 

national park into attainment by excluding the power plant from ozone control mandates that 

apply only inside the nonattainment area. Therefore, for the secondary standard, nearby should 

be defined to include anywhere within the state. 

In the context of interstate pollution, it is true that there will be CAA §§ 126 and 

110(a)(2)(D)(i)(I) to address this situation. However, in practice these tools have been extremely 

slow to achieve actual results. A much more effective and efficient approach would be to again, 

in the context of the secondary NAAQS, use a more expansive definition of nearby to go beyond 

contiguous counties. While this is a more expansive definition, it is not unprecedented. For 

example, for the 2006 PM2.5 NAAQS, EPA included non-contiguous areas in the Cincinnati 

nonattainment area to ensure that power plants that where contributing to violating monitors 

could be appropriately controlled. 

 

647 79 Fed. Reg. at 75,372. 

648 Id. 
238

In the context of the primary standard, EPA should seriously reconsider its position on a 

multistate nonattainment designation as has been repeatedly requested by Mid-Atlantic states 

such as Delaware and Maryland which receive the majority of their ozone and ozone precursors 

from upwind states on many days. EPA has repeatedly rejected these requests stating that the 

Good Neighbor provisions are the appropriate way to deal with this situation. Yet, at the same 

time, EPA has steadfastly refused to move forward with the timely implementation of the Good 

Neighbor provisions for the 2008 ozone NAAQS. This does not serve the states’ or the public’s 

interest. 

e. Background Ozone Levels

EPA includes a discussion of background ozone levels. That is, EPA claims that in some 

areas on some days, ozone and its precursors from international and natural sources could 

prevent reaching attainment levels, especially in locations with “few remaining untapped 

opportunities for local emission reductions.”649 Yet EPA acknowledges that: “modeling 

indicates that U.S. anthropogenic emission sources are the dominant

contributor to the majority of modeled O3 exceedances of the NAAQS across the U.S.”650 EPA 

also correctly notes that the Clean Air Act already contains provisions to address these situations 

in the extremely rare case that there is a credible claim.

Moreover—though it is not legally relevant, see API, 661 F.2d at 1185 (“Houston's 

argument that because natural factors make attainment impossible the Administrator acted 

arbitrarily and capriciously in setting the primary ozone standard at an ‘unattainable’ level is 

addressed in part by our analysis of API’s attainability argument. Attainability and technological 

feasibility are not relevant considerations in the promulgation of national ambient air quality 

standards.”)651 The significant cost-effective emission reductions available and resultant ambient 

air quality improvements are discussed in Part VII below. 

Background ozone levels are not the issue here. Nevertheless, air pollution needs to be 

reduced to levels that don’t harm public health, period. When EPA sets the standard, by law it 

must base that decision solely on what it takes to protect public health with an adequate margin 

of safety. In other words, the only legitimate concern is the impact on human health. 

Looking just at natural levels of ozone, spring and summer, when background levels are 

typically highest, mean levels are found to range from 15-35 ppb, including high elevation sites 

(where natural background is typically higher).652 For most locations, median levels fall between 

20 -25 ppb. Even when taking into account emissions from outside of the U.S. and during the 

spring and summer at high elevation, average background levels still do not go above 50 ppb. 653 

 

649 Proposed Rule at 75,382. 

650 Id. 

651 To the extent there is any conflict between this case and later cases like ATA III, the “earlier decision”—API—

binds. United States v. Old Dominion Boat Club, 630 F.3d 1039, 1045 (D.C. Cir. 2011).

652

 Policy Assessment at 2-13. 

653 Id. at 2-14. 
239

Background levels of ozone are typically well below air quality standards. 654 

Furthermore, it is U.S. man-made emissions that are responsible for pushing concentrations to 

levels above current and proposed air quality standards – even in high elevation areas.655 

Models estimate that background ozone contributes to between 59 and 66 percent of seasonal 

mean ozone. Even in Denver, at high elevation, man-made emissions from U.S. sources are 

responsible for about 45 percent of total ozone. 656 With nearly half, or often more, of ozone 

stemming from U.S. man-made sources, there is plenty of room to take action. 

There are rare events where background sources cause a sudden surge in ambient ozone 

levels, however, the CAA expressly plans for excluding these emissions. Section 179(b) of the 

CAA allows for exclusion of air quality data when exceedances result from international 

emissions. EPA’s exceptional events policy allows the agency to exclude ambient monitoring 

data when calculating design values, and determining attainment, when background levels from 

natural or international sources cause a spike in emissions. 

Even though background ozone levels are not a significant concern here, it is worth 

noting that EPA can’t set air quality standards based on attainability. In 1979, the City of 

Houston challenged EPA’s setting of a one-hour ozone standard at 120 ppb as being too close to 

natural background levels. This argument was rejected by the court, which found that 

attainability is not a relevant consideration in setting air quality standards and that EPA does not 

need to tailor standards to meet the needs of different locations. API v. Costle, 665 F.2d 1176, 

1185-1186 (D.C. Cir. 1981). In other words, claims that standards are hard to meet because they 

are close to background levels are nothing new and are not appropriate for EPA to consider in 

setting a health-protective standard. 

In short—background ozone levels are nowhere near proposed air quality standards and if 

there are exceptional events--cases where emissions from natural or international sources do 

result in especially high levels—there are processes by which EPA can exclude these from 

calculations. 

f. EPA Must Complete Its Reconsideration of the 2008 Ozone 

NAAQS

As discussed above in Section II.B, in 2010, EPA proposed to reconsider the 2008 

NAAQS.657 In 2011, EPA abruptly halted the reconsideration process. When several public 

health and environmental organizations challenged the decision, EPA moved for dismissal on the 

ground that it was actually just deferring its reconsideration:

EPA decided to coordinate further proceedings on its voluntary rulemaking on 

reconsideration with that ongoing periodic review, by deferring the completion of 

its voluntary rulemaking on reconsideration until it completes its statutorily-

 

654

 Background levels also fall below EPA’s proposed secondary, or welfare-based, standard of from above 15 

ppm-hrs to 7 ppm-hrs, expressed in terms of the W126 index, falling below 3 ppm-hrs. Policy Assessment at 2-21.

655 Policy Assessment at 2-20. 

656 Policy Assessment at 2-16, 2-21. 

657 75 Fed. Reg. 2,938 (Jan. 19. 2010).
240

required periodic review. Because EPA’s deferral neither concludes its voluntary 

rulemaking reconsidering the 2008 Ozone NAAQS nor establishes legal rights or 

obligations, it does not constitute judicially reviewable final agency action under 

the Clean Air Act.

EPA Mot. to Dismiss at 2, American Lung Ass’n v. EPA, No. 11-1396 (D.C. Cir. Dec. 8, 2011); 

accord id. at 11. The court granted the motion, accepting EPA’s characterization of its action as 

a “non-final decision to defer action on the 2008 voluntary revision of the national ambient air 

quality standards for ozone.” Order, American Lung Ass’n, No. 11-1396 (D.C. Cir. Feb. 17, 

2012); see also Mississippi, 744 F.3d at 1341-42 (summarizing history).

EPA has assured the D.C. Circuit that it would complete the reconsideration of the 2008 NAAQS 

along with the completion of this mandatory review. EPA must follow through on that 

commitment and conclude the reconsideration rulemaking as it promised, bearing in mind that it 

may not consider implementation costs in making determinations on the strength of the NAAQS. 

See Whitman, 531 U.S. at 468-71.

VI. THE NEW NAAQS IS, AT ITS CORE, ALSO AN ENVIRONMENTAL 

JUSTICE ISSUE: EPA MUST SET A STANDARD THAT IS PROTECTIVE 

OF MINORITIES AND ELIMINATES THE ROLE THAT OZONE PLAYS IN 

THEIR HEALTH OUTCOMES

EPA’s proposed environmental justice analysis also falls far short of an analysis that 

complies with the applicable Executive Order. Executive Order 12,898 calls for agencies to 

“identify[] and address[], as appropriate, disproportionately high and adverse human health or 

environmental effects of its programs, policies, and activities on minority populations and lowincome populations in the United States and its territories and possessions, the District of 

Columbia, the Commonwealth of Puerto Rico, and the Commonwealth of the Mariana Islands.” 

Yet EPA acknowledges that the analysis that it performed “cannot be used to draw any 

conclusions regarding potential disparities in exposure or risk across populations of interest from 

an EJ perspective.”658 Nevertheless, EPA claims that “EPA believes the human health or 

environmental risk addressed by this action will not have potential disproportionately high and 

adverse human health or environmental effects on minority, low-income or indigenous 

populations because it does not affect the level of protection provided to human health or the 

environment.”659 This statement is doubly arbitrary: first, by its own admission, EPA has no 

basis whatsoever for its stated belief; second, the claim that the ozone NAAQS “does not affect 

the level of protection provided to human health or the environment” is entirely false, for the 

NAAQS’ entire purpose is to protect public health and the environment. EPA’s claim that it has 

done any meaningful environmental justice analysis is thus astounding in its chutzpah. 

As EPA sets a new ozone NAAQS standard, it is critical that EPA carefully consider 

impacts and health outcomes in minority and lower socioeconomic communities. Minority and 

lower socioeconomic communities--which can and often do overlap—are frequently 

 

658 U.S. EPA (2014). Regulatory Impact Analysis of the Proposed Revisions to the National Ambient Air Quality 

Standards for Ground-Level Ozone (EPA-452/P-14-006 ), at 9A-1 [hereinafter RIA]; accord id. at 9A-6.

659 Proposed Rule at 75,387/1.
241

disproportionately exposed to higher levels of ozone air pollution, to more types of elevated air 

pollution and to more chronic air pollution. And, perhaps not surprisingly, minorities and lower 

socioeconomic communities suffer a disproportionately higher asthma burden in the United 

States --particularly African-Americans, Puerto Ricans, and Native Americans.

EPA has an Interim Process Guide on how to incorporate environmental justice into its 

actions.660 Notably, the Interim Process Guide explicitly contemplates a cumulative impacts 

analysis, which as discussed below is a highly important part of addressing environmental justice 

issues. EPA should utilize its Interim Process Guide and engage in a cumulative impacts 

analysis to ensure that the 2015 Ozone NAAQS standard effectively addresses environmental 

justice issues. 

A. Across the Nation Minorities Disproportionally Live in Higher Levels of 

Ozone and Thus Will Disproportionately Suffer the Impacts of an 

Insufficient Ozone Standard

Setting a new ozone standard is inescapably an issue with significant environmental 

justice implications for a number of reasons. Among other things, more minorities are over 

represented in areas with lower air quality and higher levels of air pollution that whites. More 

specifically, by cross referencing census data, EPA’s nonattainment designations for the 2008 

ozone standard, and levels of ozone (2011-2013 “design values” for the 2008 ozone standard), a 

clear and persistent trend becomes evident. 

African-Americans in particular may be at higher risk of early death from ozone pollution 

than the general population. Bell et al. (2008) 661 examined 98 urban communities in the U.S. and 

reported that the risk between ozone and mortality was greatest in areas with high 

unemployment, a higher percentage of African-Americans, higher public transportation use, and 

a lower availability of air conditioning. These results indicate that some segments of the 

population may face higher health burdens of ozone pollution. The mean long-term ozone 

concentration in this study was 26.8 ppb. 

For example, in Tennessee, blacks are approximately 30% overrepresented in areas that 

fail to meet the 2008 ozone standards, and whites are approximately 30% underrepresented in 

such nonattainment areas when compared to average state wide racial demographics. Nor is 

Tennessee alone in this dubious distinction. In the South alone, Alabama, Arkansas, North 

Carolina, Georgia, Kentucky and Texas all have higher relative concentrations of blacks—

sometimes far higher--living in areas that fail to meet the minimum ozone standards than 

concentrations of whites. This is reflected in the graphs below.

 

660 See EPA’s Action Development Process: Interim Guidance on Considering Environmental Justice During the 

Development of an Action, http://www.epa.gov/environmentaljustice/resources/policy/considering-ej-inrulemaking-guide-07-2010.pdf; see also EPA, Draft Technical Guidance for Assessing Environmental Justice in 

Regulatory Analysis, http://www.regulations.gov/#!docketDetail;D=EPA-HQ-OA-2013-0320.

661M.L. Bell & F. Dominici (2008). Effect modification by community characteristics on the short-term effects of 

ozone exposure and mortality in 98 US communities, Am. J. Epidemiol., 167: 086-997. 
242
243
244

The same holds true for central and mid-west states. As reflected in the graphs below, 

Wisconsin, Illinois, Michigan, Missouri, Ohio, Kansas, and Oklahoma are particularly notable in 

the over representation of blacks living in areas that fail to meet minimum air quality standards 

for ozone. Nevada also follows this trend.
245
246
247

The trend can also be seen in eastern and mid-Atlantic states, where Pennsylvania and 

Rhode Island have higher relative exposures among blacks than whites, though in other states 

such as New York and Virginia minorities that are at greater relative exposure than whites are 

Hispanics and Asians. 
248

 
249

Indeed, as the line graphs below demonstrate, for many states there is a striking 

correlation between increasing concentrations smog, increasing concentrations of minorities and 

decreasing concentrations of whites in areas that fail to meet minimum air quality standards. 

Stated another way, as air quality progressively worsens, representation of blacks and other 

minorities in the population increases while representation of whites in the population decreases. 
250
251
252
253

B. Setting An Ozone Standard That Protects Environmental Justice 

Communities Requires EPA To Consider The Cumulative Impacts Including 

Synergistic Exposures To Multiple Pollutants 

It is critical to consider the cumulative impacts of multiple stressors when assessing 

health impacts, including a population’s exposure to multiple pollutants, exposure to higher 

levels of multiple pollutants, and chronic exposure to lower levels of multiple pollutants. This is 

particularly important if the 2015 Ozone NAAQS is to adequately address environmental justice 

issues, as it must.

As CASAC noted in its June 2014 letter to EPA concerning the promulgation of the 2015 

ozone NAAQS: 

EPA should consider how review and revision of the NAAQS can be done 

synergistically for logical, scientifically relevant groupings of criteria pollutants. 

For example, O3 and NO2 are both criteria pollutants that are inter-related via 

atmospheric chemistry, and human exposure to these pollutants is often in the 

form of a mixture that includes both, and other pollutants such as particulate 

matter. The National Research Council and the North American Research 

Strategy for Tropospheric Ozone have both made detailed recommendations for 
254

multipollutant approaches to air quality management. . . CASAC encourages EPA 

to explore multipollutant approaches for review of the primary standards . . .662

This is particularly true when evaluating sensitive sub-groups such as minority 

communities and low-income communities that frequently experience higher exposure to air 

pollution and disproportionate impacts.663 Minorities and lower income communities are more 

likely to live or work near pollution sources and to have higher pollution burdens from mobile 

and stationary sources, which are only exacerbated by factors such as health care access, housing 

market dynamics, and predisposed traits. 664 These higher pollution burdens are associated with 

health outcomes such as respiratory and cardiovascular disease, low birth weight, and premature 

mortality.665 

Epidemiological studies similarly suggest that socioeconomic status (“SES”) is 

associated with higher risks of ozone-related health outcomes.666 EPA concludes that “most 

studies of individuals have reported that individuals with low SES and those living in 

neighborhoods with low SES are more at risk for O3-related health effects, resulting in increased 

risk of respiratory hospital admissions and ED visits.”667 For example, a New York City study 

showed that children with lower socioeconomic status had greater risk of ozone-induced hospital 

admissions for asthma.668 Accordingly, the ISA noted that “evidence is suggestive of SES as a 

factor affecting risk of O3-related health outcomes.”669

To be sure, controlled human exposure studies are valued for their ability to control and 

eliminate confounding factors such as temperature, co-pollutants, or allergens and the 

epidemiological studies EPA relies upon are subjected to rigorous statistical analysis to control 

for confounding effect of multiple pollutant exposures.670 Yet in the real world, physiological 

impacts are likely to be even worse than what is experienced in the exposure studies because of 

the addition of these other factors. The combined effects among air pollutants produce important 

 

662 CASAC Letter 2014a at v.

663 Policy Assessment at 1-15; ISA at 8-1, 8-2, 8-2.

664 Morello-Frosch et al. (2011). Understanding the Cumulative Impacts of Inequalities in Environmental Health: 

Implications for Policy, Health Affairs, 30(5): 879-887.

665 American Lung Association, State of the Air-Disparities in the Impact of Air Pollution (2013), available at

http://www.stateoftheair.org/2013/health-risks/health-risks-disparities.html#_ftn1.

666 S. Lin, X. Liu, L.H. Le, & S. Hwang (2008). Chronic exposure to ambient ozone and asthma hospital admissions 

among children, Env. Health Perspect., 116(12): 1725-1730.; J.T. Lee, J.Y. Son, H. Kim, & S.Y. Kim (2006). Effect 

of air pollution on asthma-related hospital admissions for children by socioeconomic status associated with area of 

residence, Arch. Environ. Occup. Health, 61(3): 123-120; S. Cakmak, R.E. Dales, M.A. Rubio, M& C.B. Vidal 

(2011). The risk of dying on days of higher air pollution among the socially disadvantaged elderly, Environ. Res., 

111(3): 388-393; M. Pastor, R. Morello-Frosch, & J. Sadd (2010). Air Pollution and Environmental Justice: 

Integrating Indicators of Cumulative Impact and Socio-Economic Vulnerability into Regulatory Decision-Making, 

California Air Resources Board. 

667 ISA at 8-27. 

668 Lin. et al. 2008, supra note 654.

669 Id. at 8-28.

670 See Proposed Rule at 75,251: “Most O3 effect estimates for lung function were robust to adjustment for 

temperature, humidity, and copollutants such as PM2.5, PM10, NO2, or SO2.”
255

physiological effects. 671 Air pollutants are inhaled as a mixture of different sources, yet focus 

has historically been placed on monitoring and regulating individual pollutants in isolation.672 

Research is beginning to show how the cumulative effects of environmental stressors can 

work to produce health disparities and regulatory agencies, including EPA, have begun 

considering ways of addressing cumulative impacts in decision-making.673 As EPA notes, 

“For example, although exposure to ozone may primarily target the respiratory 

system, "real-world" combined exposures to particulate matter, ozone and 

hazardous air pollutants may affect multiple target organs. Multipollutant 

exposures may elicit acute, adaptive responses across the respiratory, cardiac, 

vascular, immunologic, neurological and other organ systems.”674

In taking a precautionary approach to protect the health of at-risk groups, EPA should not 

consider ozone exposure in isolation, but should also consider the combined burdens of multipollutant exposure and additional environmental stressors. Indeed, doing so is consistent with 

EPA’s mandate to set a NAAQS standard that protects the public health with an adequate margin 

of safety. And EPA can use its cumulative impacts framework as a roadmap for doing so.675 

C. The Environmental Justice Implications of Setting the 2015 NAAQS Are 

Evident in the Asthma Burdens of Minorities, Including in Particular 

African-Americans 

The environmental justice implications of the 2015 Ozone NAAQS is evident in the 

asthma burdens of minority populations. To be sure, ozone is not the only cause of asthma, nor 

the only thing that can trigger an asthma attack. However, research has shown that it is an 

important cause of asthma incidence, prevalence and attacks. As such, the level of ozone that 

EPA decides to allow under the 2015 Ozone NAAQS is clearly of immediate and direct 

importance to the health of environmental justice communities. 

In absolute number terms, African-Americans are most heavily burdened by asthma in 

the U.S. Nationally, the current asthma prevalence rate for non-Hispanic blacks is 11.9%, 

compared to 8.1% for non-Hispanic whites and 7.0% for Hispanics.676 While the prevalence rate 

reflects a relatively significant disparate impact, it actually understates asthma’s true burden on 

the African-American community. Other key statistical measures of asthma’s impact – including 

 

671 J. Mauderly& J. Samet (2009). Is there Evidence for Synergy Among Air Pollutants in Causing Health Effects?, 

Environ. Health Perspect., 117(1):1-6; ISA sec. 4.3.4.

672 U.S. EPA, Exposure and Health Effects of Mixtures of Air Pollutants, available at 

http://www2.epa.gov/air-research/exposure-and-health-effects-mixtures-air-pollutants (accessed Mar. 16, 2015).

673 D.O. Johns et al. (2012). Practical Advancement of Multipollutant Scientific and Risk Assessment Approaches 

for Ambient Air Pollution, Env. Health Perspectives, 120(9): 1238-1242 (2012). 

674 U.S. EPA, Exposure and Health Effects of Mixtures of Air Pollutants.

675 See U.S. EPA (2003), Framework for Cumulative Risk Assessment (EPA/630/P-02/001F) available at 

http://www2.epa.gov/sites/production/files/2014-11/documents/frmwrk_cum_risk_assmnt.pdf.

676 CDC, Asthma Surveillance Data, available at http://www.cdc.gov/asthma/asthmadata.htm (accessed Mar. 13, 

2014).
256

hospitalization rates, emergency department visit rates, and mortality rates – show a much 

starker contrast. These other measures typically show disproportionate impacts of approximately 

200-400% when comparing non-Hispanic blacks to non-Hispanic whites. The following table, 

which includes statistics from states that have recent data in at least three of the four major 

categories, illustrates this pattern: 

State Current Prevalence 

among Adults

Hospitalization 

Rate*

Emergency 

Department Visit 

Rate* 

Mortality Rate*

White 

NonHispani

c

Black 

NonHispani

c

White 

NonHispani

c

Black 

NonHispani

c

White 

NonHispani

c

Black 

NonHispani

c

White 

NonHispani

c

Black 

NonHispani

c

Connecticut

677

8.3% 15% 86 405 342 1273 0.77 2.61

Texas678 9.2% 10.2% 88 195 N/A N/A 1.0 1.9

North 

Carolina679

7.2% 10% 75 210 N/A N/A 0.68 1.8

Indiana680 8.7% 13.7% 85 306 344 1293 N/A** N/A**

Wisconsin681 8.6% 15.9% 63 346 N/A N/A 0.79 3.54

* Per 100,000 persons

**Indiana data provides raw mortality numbers but not mortality rates. In 2011, 73 Indiana residents died from 

asthma, 54 of whom were white and 18 of whom were black. African-Americans thus comprised approximately 

24% of asthma deaths despite accounting for only 9% of Indiana’s total population. 

As the data summarized in the table above shows, asthma’s disproportionate impact is 

greater for the most serious, life-threatening asthma-related complications. In Wisconsin, the 

mortality rate for non-Hispanic blacks is nearly 450% higher than the mortality rate for nonHispanic whites. Connecticut’s hospitalization rate discrepancy is also well over 400%. Even 

the states listed above that have the most equitable asthma burdens – North Carolina and Texas –

have near or over a 200% discrepancy in both hospitalization rates and mortality rates. Stated 

another way, current prevalence rate is a measure of who has been recently diagnosed with 

asthma, while the other statistical categories are measures of who suffers the worst asthmarelated complications (those complications that necessitate hospital visits or result in death). 

And the data shows that not only are African Americans more likely to have asthma, but even 

among asthma sufferers, they are more likely to have worse outcomes: not all individuals who 

 

677 Connecticut Dept. of Health (2012). The Burden of Asthma in Connecticut 2012 Surveillance Report, available 

at http://www.ct.gov/dph/lib/dph/hems/asthma/pdf/full_report_with_cover.pdf.

678 Texas Dept. of State Health Services, Asthma Health Facts 2011, available at 

https://www.dshs.state.tx.us/asthma/data.shtm#New_Asthma (accessed Mar. 13, 2014),.. 

679 North Carolina Dept. of Health and Human Services (2010).The Burden of Asthma in north Carolina 2010, 

available at http://www.asthma.ncdhhs.gov/docs/TheBurdenOfAsthmaInNorthCarolina-2010.pdf; North Carolina 

Dept. of Health and Human Services, African Americans and Asthma in North Carolina (Mar. 12, 2014), 

http://www.asthma.ncdhhs.gov/docs/factsheets/2011/AfricanAmericansAndAsthmaInNorthCarolina.pdf. 

680 680 Indiana State Dept. of Health, Asthma Fact Sheet, available at 

http://www.in.gov/isdh/files/ISDH_FactSheet_Asthma_Nov2013_FINAL(1).pdf (accessed Mar. 123, 2014).

681 Wisconsin Dept. of Health (2013). Burden of Asthma in Wisconsin 2013.
257

have asthma suffer from it equally. A higher percentage of African-Americans have asthma, but 

an even higher percentage suffer from its most serious symptoms and complications. 

Minority groups other than African-Americans are also disproportionately affected by 

asthma. Nationally, Puerto Ricans and American Indians/Native Alaskans have a much higher 

current asthma prevalence rate than even African-Americans, at 16.7% and 14.3% 

respectively.682 683 In Hawaii, the prevalence rate for Native Hawaiians is 14.9%, compared to 

only 9.0% for whites living in Hawaii.684 Asthma’s heavy burden on these groups is also evident 

from other statistical measures. Nationally, the mortality rate for Puerto Ricans is four times 

higher than the mortality rate for whites.685 Similar trends exist at the state level for Native 

Americans. In Oregon and Wisconsin, for example, the American Indian hospitalization rate is 

double the rate for non-Hispanic whites.686 And while asthma prevalence among the total 

Hispanic population is actually lower than the national average, Hispanics also have higher 

hospitalization and mortality rates than non-Hispanic whites, and thus also suffer 

disproportionately.687 Hispanics are 30% more likely to visit the hospital for asthma, as 

compared to non-Hispanic whites, and Hispanic children are 40% more likely to die from 

asthma.

As is evident from the statistics, asthma has an extremely disproportionate impact on 

minorities across all parts of the United States. It is undisputed that ozone is a trigger for asthma 

attacks. And the ozone standard that CASAC and EPA develop must be protective of minorities 

and eliminate the role that ozone plays in the above health outcomes.

VII. ADDITIONAL CONSIDERATIONS

A. Emission Reductions Needed to Improve Air Quality Are Readily Available

As discussed in Section II above, the Supreme Court has been absolutely clear that the 

primary NAAQS must be established based on health considerations alone and must not be based 

on cost or technological feasibility. Whitman v. Am. Trucking Ass’ns, 531 U.S. 457, 464-71 

(2001); see also Am. Lung Ass’n v. EPA, 134 F.3d at 389 (Administrator must promulgate 

national standards that limit emissions sufficiently to establish that margin of safety “without 

reference to cost or technological feasibility”). Even if they were relevant, however, industry 

statements regarding both the feasibility of meeting a lower ozone standard and the costs of 

doing so are greatly overstated. Significant cost-effective VOC and NOx reductions are readily 

 

682 The Office of Minority Health, Asthma and American Indians/Alaskan Natives, available at 

http://minorityhealth.hhs.gov/templates/content.aspx?lvl=3&lvlID=532&ID=6172 (accessed Mar. 13, 2014).

The Office of Minority Health, Asthma and Hispanic Americans, available at 

http://minorityhealth.hhs.gov/templates/content.aspx?lvl=3&lvlID=532&ID=6173 (accessed Mar. 13, 2014),.. 

684 Hawaii State Dept. of Health, Hawai’i Asthma Plan 10 (2013).

685 The Office of Minority Health, Asthma and Hispanic Americans (Mar. 13, 2014), 

http://minorityhealth.hhs.gov/templates/content.aspx?lvl=3&lvlID=532&ID=6173.

686 Oregon Health Authority, Asthma Emergency Department Visits and Hospitalizations (Mar. 12, 2014), available 

at https://public.health.oregon.gov/DiseasesConditions/ChronicDisease/Asthma/Documents/burden/ch7.pdf (Mar. 

12, 2014); Wisconsin Dept. of Health 2013, supra.

687 The Office of Minority Health, Asthma and Hispanic Americans, supra. 
258

available using available and proven control technologies, many of which are already employed 

on major emission sources and are simply not being operated consistent with best prior levels. 

1. Significant Emission Reductions Are Already Underway and Further 

Emission Reductions Are Readily Achievable

Ozone forms when nitrogen oxides and volatile organic compounds react in the presence 

of heat and sunlight. Over 70% of annual NOx emissions in the United States come from two 

source sectors: mobile sources and coal fired power plants.688 Significant emission reductions 

are already underway in both of these source sectors due to the ongoing implementation of 

existing rules and the turnover of the vehicle fleet. 

EPA in multiple rulemakings has identified significant reductions in ozone levels that are 

occurring and will continue across the country. In its Regulatory Impact Analysis for the CrossState Air Pollution Rule (CSAPR), EPA projected that in the absence of the rule, total NOx 

would decline by over 7 million tons between 2005 and 2014, that EGU NOx would decline 

from over 3.7 million tons to under 2.1 tons, and that the rule would drive an incremental 

200,000 tons of annual NOx reductions.689 EPA stated that these “significant aggregate 

reductions” in EGU NOx emissions “would lower overall ambient levels of . . .ozone across 

much of the eastern U.S.”690 Due to litigation delays, these emission reductions have not been 

fully implemented to date, so additional reductions from CSAPR can be anticipated over the next 

two years.691

Also in the EGU sector, implementation of the Best Available Retrofit Technology 

(BART) and Reasonable Further Progress (RFP) requirements of the regional haze provisions of 

the Clean Air Act have resulted State and Federal Implementation Plans are driving significant 

further reducing emissions of NOx. BART and RFP requirements are driving numerous control 

installations of Selective Catalytic and Selective Non-Catalytic Reduction (SCR and SNCR) 

technology. BART determinations for the following units drove installation of SCR or SNCR. 

Table 30: BART Determinations Driving SCR or SNCR

State Facility BART determ.

AZ AEPCO Apache Unit 2 Gas conversion

AZ AEPCO Apache Unit 3 SNCR

AZ APS Cholla Unit 2 SCR + LNB/OFA

AZ APS Cholla Unit 3 SCR + LNB/OFA

AZ APS Cholla Unit 4 SCR + LNB/OFA

 

688 U.S. EPA, 2011 National Emission Inventory, available at http://www.epa.gov/ttnchie1/net/2011inventory.html. 

689 U.S. EPA, Office of Air and Radiation, Regulatory Impact Analysis for the Federal Implementation Plans to 

Reduce interstate Transport of Fine Particulate Matter and Ozone in 27 States; Correction of SIP Approvals for 22 

States, 51 Tbl. 3-7, 55 Tbl. 3-10 (June 2011).

690 Id. at 74. 

691 In December 2014, EPA issued rulemaking establishing a revised implementation schedule for CSAPR, which 

shifted CSAPR’s original 2014 compliance deadline out to 2017. See EPA, Rulemaking to Amend Dates in Federal 

Implementation Plans Addressing Interstate Transport of Ozone and Fine Particulate Matter, 79 Fed. Reg. 71,663 

(Dec. 3, 2014). (See Exhibit 22). 
259

AZ SRP Coronado Unit 1 SCR + LNB/OFA

AZ SRP Coronado Unit 2 SCR + LNB/OFA

CO Craig Station 1 SCR + existing LNB/OFA

CO Craig Station 2 SCR + existing LNB/OFA

CO Hayden Station 1 SCR

CO Hayden Station 2 SCR

MT Colstrip 1 SOFA+SNCR

MT Colstrip 2 SOFA+SNCR

ND Coal Creek Unit 1 & Unit 2 LNB+SOFA+SNCR

ND Leland Olds 1 SNCR + Basic SOFA

ND Leland Olds 2 SNCR + ASOFA

ND Milton R. Young 1 SNCR + ASOFA

ND Milton R. Young 2 SNCR + ASOFA

ND Stanton 1 with Lignite Coal LNB+OFA+SNCR

ND Stanton 1 with Powder River Basin Coal LNB+OFA+SNCR

NM Four Corners 1 Shutdown

NM Four Corners 2 Shutdown

NM Four Corners 3 Shutdown

NM Four Corners 4 SCR

NM Four Corners 5 SCR

NM San Juan Generating Station Unit 1 SNCR

NM San Juan Generating Station Unit 2 Shutdown

NM San Juan Generating Station Unit 3 Shutdown

NM San Juan Generating Station Unit 4 SNCR

NV Reid Gardner 1 ROFA + Rotamix or LNB+OFA+SNCR

NV Reid Gardner 2 ROFA + Rotamix or LNB+OFA+SNCR

NV Reid Gardner 3 ROFA + Rotamix or LNB+OFA+SNCR

NV Tracy 3 LNB + SNCR

WA TransAlta Centralia Units 1 and 2 Flexfuel + SNCR

WY Dave Johnson Unit 3 SCR or shutdown

WY Laramie River Unit 1 SCR

WY Laramie River Unit 2 SCR

WY Laramie River Unit 3 SCR

WY Laramie River Unit 4 SCR

WY Naughton Unit 3 SCR

Although these decisions are driving reductions in NOx as a condensable to fine particulate 

matter that mars vistas in our national parks and wilderness areas, the NOx reductions resulting 

from these BART and RFP determinations will have significant benefits for ozone formation as 

well. 
260

In addition, the Mercury and Air Toxics Standard, while not directly targeting reductions 

in NOx emissions has nevertheless led a number of older, highly polluting facilities to elect to 

retire rather than upgrade outdated emission control systems for mercury and other hazardous air 

pollutants, with attendant benefits for NOx emissions. 

Although not yet final, there are significant synergies between a low ozone standard and 

the Clean Power Plan (CPP), which projects large reductions in NOx emissions. EPA expects 

the CPP to have the following estimated human health co-benefits:

In addition to CO2, implementing these proposed guidelines is expected to reduce 

emissions of SO2 and NOX, which are precursors to formation of ambient PM2.5, 

as well as directly emitted fine particles. Therefore, reducing these emissions 

would also reduce human exposure to ambient PM2.5 and the incidence of 

PM2.5-related health effects. In addition, in the presence of sunlight, NOX and 

VOCs can undergo a chemical reaction in the atmosphere to form ozone. 

Depending on localized concentrations of volatile organic compounds (VOCs), 

reducing NOX emissions would also reduce human exposure to ozone and the 

incidence of ozone-related health effects.692

According to EPA estimates, the CPP is projected to reduce emissions of pollutants that 

contribute to ground-level ozone by over 25 percent in 2030.693 This includes emission 

reductions of 407,000 to 428,000 tons of nitrogen dioxide694 and 128,000 tons of ozone-season 

NOX in 2030.695 Thus, costs of implementing the CPP should be appropriately excluded from 

cost estimates of a 60 ppb ozone standard.

In the mobile source context, further reductions will be achieved as the nation's vehicle 

fleet becomes more efficient, cleaner, and electrified. California has been at the cutting edge of 

cleaning up emissions from vehicles. At least 14 states have adopted California’s Clean Car 

Standards, which in addition to reducing greenhouse gas emissions from passenger vehicles, 

achieve significant reductions in NOx and VOCs as well.696 In those states, the standards 

become effective for vehicles with model years between 2005 and 2011,697 meaning that ongoing 

fleet turnover will continue to drive improvements in vehicle fleet emission of ozone precursors. 

EPA’s Tier 3 Vehicle Emission and Fuel Standards Program (Tier 3) (see Exhibit 23 and 

24) is anticipated to have huge benefits for reducing NOx and VOC emissions. EPA predicts 

 

692 U.S. EPA, Regulatory Impact Analysis for the Proposed Carbon Pollution Guidelines for Existing Power Plants 

and Emission Standards for Modified and Reconstructed Power Plants, 4-14 (June 2014).

693 U.S. EPA, EPA Fact Sheet: Clean Power Plan, available at http://www2.epa.gov/sites/production/files/2014-

06/documents/20140602fs-important-numbers-clean-power-plan.pdf

694 Id.

695 U.S. EPA, Memorandum: Emission Reductions, Costs, Benefits, and Economic Impacts Associated With 

Building Blocks 1 and 2 

696 In order of adoption: New Jersey, Connecticut, Washington, Vermont, New York, Maine, Rhode Island, 

Massachusetts, Oregon, Arizona, Pennsylvania, Maryland, Florida, and New Mexico. See Maryland Department of 

the Environment, States Adopting California’s Clean Cars Standards,, available at 

http://mde.maryland.gov/programs/Air/MobileSources/CleanCars/Pages/states.aspx. 

697 Id.
261

that upcoming Tier 3 standards will reduce onroad NOx emissions—the largest single category of 

NOx emissions—by nearly 10% in 2018, 25% by 2030, and 80% by 2050. 698 For VOCs, EPA 

predicts a 3% reduction by 2018, 16% by 2030, and 28% by 2050.699 EPA projects that by 2018, 

Tier 3 will reduce ozone design values substantially against a 2018 reference case in certain key 

urban areas.700 For example, the design values in Washington D.C. and surrounding counties in 

2018 are anticipated to be decreased by over 1 ppb701 and the design values for many counties in 

the Atlanta area approaches or exceeds 1.5 ppb.702 Benefits are anticipated to be even greater by 

2030. For example, the modeled design values in the Washington D.C. metro in 2030 are 

decreased by more than 2.5 ppb in 2030 compared to the reference case,703 and decrease by 

nearly 3.0 ppb in 2030 compared to the reference case in the metro Atlanta area.704

Catalytic converter technology is now capable of eliminating over 95% of NOx emissions 

from on-road passenger vehicles. As the California Air Resource Board (CARB) explained eight 

years ago: 

Current catalytic converter designs are more than 95% efficient in removing the 

hydrocarbons (HC), carbon monoxide (CO), and oxides of nitrogen (NOx) from 

engine exhaust before they reach the atmosphere. Improvements in catalytic 

converter washcoats, precious metal loading, and substrate designs over the years, 

in combination with better vehicle fuel control systems, are the primary factors 

that have made compliance with California’s very low emission standards 

possible.705

New York adopted the CARB standards for aftermarket catalytic converters in 2013706 and 

Maine adopted the CARB standards, although has delayed implementation until 2018.707 As 

catalytic converters achieving these high levels of emission reductions are more widely 

employed on new vehicles, and as the fleet turns over, there will be further reductions in NOx 

emissions from the mobile source sector. 

 

698 U.S. EPA (2014). Office of Transportation and Air Quality, Regulatory Impact Analysis: Control of Air Pollution 

from Motor Vehicles: Tier 3 Motor Vehicle Emission and Fuel Standards Final Rule, 7-48.

699 Id., 7-49.

700 U.S. EPA (2014). Air Quality Modeling Technical Support Document: Tier 3 Motor Vehicle Emission and 

Standards (EPA-454/R-14-002), Appendix B: 8-Hour Ozone Design Values for Air Quality Modeling Scenarios.

701 Id.

702 See id. (Cobb County, GA: 1.28 ppb; De Kalb County, GA: 1.43 ppb; Douglas County, GA: 1.27 ppb; Fayette 

County, GA: 1.39 ppb; Gwinnett County, GA: 1.51 ppb; Henry County, GA: 1.56 ppb)

703 See id. (Washington, D.C.: 2.73 ppb; Montgomery County, MD: 2.40 ppb; Prince Georges County, MD: 1.87 

ppb; Arlington County, VA: 2.70 ppb; Fairfax County, VA: 2.68 ppb; Alexandria City, VA: 2.50 ppb).

704 See id. (Cobb County, GA: 2.35 ppb; De Kalb County, GA: 2.74 ppb; Douglas County, GA: 2.08 ppb; Fayette 

County, GA: 2.45 ppb; Gwinnett County: 2.82 ppb; Henry County, GA: 2.54 ppb)

705 State of California Air Resources Board, Staff Report: Initial Statement of Reasons for Rulemaking, Public 

Hearing to Consider Amendments to Regulations Regarding New Aftermarket Catalytic Converters and Used 

Catalytic Converters Offered for Sale and Use in California (Sept. 7, 2007). (See Exhibit 25).

706 See New York State Dept. of Env. Conservation, Fact Sheet Prohibition of Used Catalytic Converters/New 

Aftermarket Catalytic Converter Standards, available at

http://www.dec.ny.gov/chemical/87411.html.

707 See Maine Dept. of Env. Protection, Rulemaking Fact Sheet (5 MRSA §8057), available at 

http://www.maine.gov/tools/whatsnew/attach.php?id=635480&an=1. (See Exhibit 26).
262

Additional reductions in ozone precursors can be achieved through increased 

electrification of the vehicle fleet. President Obama in 2008 set a goal of 1 million electric 

vehicles (EVs) on the road by 2015.708 According to data from the Electric Drive Transportation 

Association, sales of plug-in vehicles have increased significantly in recent years.709

Table 31

Year Plug-in Vehicle 

Salesa

2014 118,773

2013 96,702

2012 52,835

2011 17,735

2010 345

a

= Includes plug-in hybrid electric vehicles and extended-range electric vehicles

The benefits of electrification of the vehicle fleet depend, of course, on reducing the 

NOx-intensity of the power generation sector. However, there are a number of reasons why the 

NOx-intensity of power generation will continue to decline. New generation comprises almost 

exclusively NOx-free renewable and relatively low-NOx new gas generation, displacing older, 

dirtier units. Moreover, the share of new generation from NOx-free renewables has been 

dramatically increasing in recent years. According to a recently-released National Renewable 

Energy Laboratory (NREL) analysis, “In 2013, renewable electricity accounted for more than 

61% of all new electricity capacity installations in the United States.”710 As cleaner, largely 

NOx free generation replaces our oldest and dirtiest power plants, the ozone benefits of vehicle 

electrification will continue to increase. 

Finally, it is important to bear in mind that societal changes and changes in patterns of 

urban development will also reduce the cost of compliance with a new ozone standard. As urban 

areas become denser, public transit improves, ride-sharing options increase, and cities become 

more walkable and bikable, reliance on NOx and VOC-emitting motor vehicles will decrease. 

2. Further Reductions in VOC Emissions from the Oil and Gas Sector 

Are Forthcoming

EPA has also taken recent steps to limit VOC emissions from the oil and gas sector. In 

2012, the agency finalized new source performance standards (NSPS) for specified equipment in 

the oil and gas industry that will reduce VOC emissions by approximately 190,000 tons annually 

starting in 2015.711 Taking into account voluntary emission reductions anticipated through 

EPA’s Natural Gas STAR program, this figure increases to 290,000 tons annually.712 The 

 

708 See U.S. White House, FACT SHEET: President Obama’s Plan to Make the U.S. the First Country to 

Put 1 Million Advanced Technology Vehicles on the Road, available at

www.whitehouse.gov/sites/default/files/other/fact-sheet-one-million-advanced-technology-vehicles.pdf. 

709 Electric Drive Transportation Association, Electric Drive Sales Dashboard, available at

http://electricdrive.org/index.php?ht=d/sp/i/20952/pid/20952. (See Exhibit 27). 

710 National Renewable Energy Laboratory, 2013 Renewable Energy Data Book at 4 (released Jan. 2015).

711 77 Fed. Reg. 49,490, 49,533 (Aug. 16, 2012).

712 Id. at 49,534.
263

measures required under the oil and gas NSPS include (but are not limited to) reduced emission 

completions (RECs) at new hydraulically fractured natural gas wells, steep cuts in emissions at 

new storage tanks, and the installation of lower-emitting designs for new compressors and 

pneumatic controllers in various segments of the industry.713 Notably, the REC component of 

the rule—the largest driver of its emission reductions—did not take effect until January 1, 

2015.714 Accordingly, the full scope of the rule’s benefits is only now materializing.

Furthermore, the White House and EPA recently announced plans for a strategy to reduce 

the oil and gas industry’s emissions of methane, a potent greenhouse gas that is often released 

into the atmosphere concurrently with VOCs.715 As part of its methane control strategy, the 

administration expects to issue another NSPS for oil and gas sources targeting methane 

emissions from new equipment not covered under the 2012 rule, which may include 

“completions of hydraulically fractured oil wells, pneumatic pumps, and leaks from new and 

modified well sites and compressor stations.”716 EPA plans to publish a proposed rule in the 

summer of 2015 and a final rule in 2016.717 

The agency also expects to develop “control technique guidelines” under section 183b of 

the Clean Air Act for existing oil and gas systems in ozone non-attainment areas and states in the 

Ozone Transport region.718 These guidelines will help affected states achieve the ozone NAAQS 

by “provid[ing] an analysis of the available, cost-effective technologies for controlling VOC 

emissions from covered oil and gas sources”719 and by establishing a “presumptive norm” for 

RACT determinations in their non-attainment SIPs. Connecticut Fund for Envt., Inc. v. E.P.A., 

672 F.2d 998, 1003 (2d Cir. 1982). The administration’s other forthcoming actions to reduce 

methane pollution from oil and gas sources, such as EPA rules requiring leak detection and 

repair and BLM rules targeting waste and flaring of natural gas on federal land, can also be 

expected to reduce co-occurring emissions of VOCs.

3. There are Significant, Economic Reductions to Be Achieved from 

Coal Fired Electricity Generating Unites in the Electric Power Sector

Despite the ongoing progress in the electric power sector, massive emission reductions 

are still readily achievable from the U.S. coal fleet. According to EPA’s 2011 National Emission 

Inventory, over 85% of electric sector NOx emissions are from coal plants.720 Although 

 

713 See id. at 49,496-99.

714 Id. at 49,492.

715 See Press Release, The White House, FACT SHEET: Administration Takes Steps Forward on Climate Action 

Plan by Announcing Actions to Cut Methane Emissions (Jan. 14, 2015), available at

http://www.whitehouse.gov/the-press-office/2015/01/14/fact-sheet-administration-takes-steps-forward-climateaction-plan-anno-1; U.S. EPA, Press Release: EPA’s Strategy for Reducing Methane and Ozone-Forming Pollution 

from the Oil and Natural Gas Industry (Jan. 14, 2015), available at

http://yosemite.epa.gov/opa/admpress.nsf/0/BA7961BF631C87BF85257DCD00526FF7

716 Press Release, EPA (Jan. 14. 2015), supra .

717 Id.

718 Id.

719 Id.

720 U.S. EPA, National Emissions Inventory, available at http://www.epa.gov/ttnchie1/net/2011inventory.html. 

Approximately 1.8 million out of 2.1 million tons of electric sector NOx were from coal-fired electric generating 

units. 
264

adoption of SCR control technology has become increasingly widespread on U.S. coal plants, 

with 327 coal units having installed SCR or having announced plans to install SCR (representing 

nearly 42% of units 100 MW or larger and over 177 GW or 56% of coal capacity),721 significant 

further progress is achievable. There are still 451 coal units accounting for 140 GW of capacity 

that lack SCR or plans to install SCR. 

More insidiously, many of the plants that have installed SCR controls, often at the 

expense of ratepayers, are not operating these controls at previously demonstrated control levels. 

In 2013, more than 20 coal units had annual NOx emission rates that were over five times greater

than their best consistently demonstrated historical emission rate (“best demonstrated emission 

rate”).722 In other words, these facilities emitted five times as much NOx in 2013 as they could 

have if they had simply operated their SCR at proven control efficiencies. More than 50 coal 

units had annual NOx emission rates that were over three times greater than their best 

demonstrated emission rate.723 At least 88 coal units had NOx emission rates that were more 

than double their best demonstrated emission rate.724 At least 135 coal units had NOx emission 

rates more than 50% higher than their best demonstrated rate.725 And over 170 units had NOx 

emission rates more than 25% higher than their best previously demonstrated rate.

726

 In other 

words, coal plants around the country have been routinely turning down their existing NOx 

emission controls—emission controls often directly paid for (with interest) by ratepayers—

causing the public to pay not only with their pocketbooks but also with their lungs. 

The consequences for NOx emissions and air quality are staggering. As documented in 

the accompanying analysis by Dr. Ranajit Sahu, if coal units that have already installed SCR 

controls simply operated those controls to replicate best demonstrated control efficiency, they 

could reduce annual ozone season emissions by more than 136,000 tons and overall annual 

emissions by more than 296,000 tons each year. Given that total coal EGU NOx emissions in 

2011 were approximately 1.8 million tons, it follows that emissions from the largest stationary 

source sector of NOx emissions could be reduced by 1/6th simply by operating existing emission 

controls. 

 

The emission reductions achievable from cleaning up the other half of the coal fleet are 

also enormous. We analyzed emissions from coal plants in CSAPR states and New England727

 

721 Compiled using data from Energy Information Agency Form 860 and EPA’s Clean Air Markets Database 

(ampd.epa.gov/ampd/). 

722 Best demonstrated historical rate was calculated by looking at daily average NOx rates reported by the facility to 

EPA and available from EPA’s Air Markets Program Database (ampd.epa.gov/ampd/) and identifying, postinstallation of SCR, the lowest NOx emission rate that was achieved on a daily basis for 30 consecutive operating 

days. Because this analysis required the facility to have met the rate as a daily average every day during a 30 

consecutive operating day period, it is a very conservative rate, especially when compared to an annual average. 

Additional data on average 2013 NOx rate was also retrieved from EPA’s Air Markets Program Database. 

723 Data from EPA’s Air Markets Program Database.

724 Id.

725 Id.

726 Id.

727 Alabama, Arkansas, Connecticut, Delaware, Florida, Georgia, Illinois, Indiana, Iowa, Kansas, Kentucky, 

Louisiana, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, Missouri, Nebraska, New Hampshire, New 

Jersey, New York, North Carolina, Ohio, Oklahoma, Pennsylvania, South Carolina, Tennessee, Texas, Virginia, 

West Virginia, and Wisconsin. (Note that Maine, Rhode Island and Vermont have no coal plants.)
265

using publicly available emission data. During the ozone season of 2011, coal plants in these 

states emitted over 570,000 tons. These ozone season emissions could be reduced by 61% 

(350,000 tons) through operation of existing controls, as described above, and installation of 

SCR controls on the remaining coal units.728 This figure excludes emissions from coal plants 

that have ceased operating between 2011 and present.729 Annual emission reductions are even 

greater: NOx emissions from these states could be reduced by nearly 780,000 tons each year 

(from 1.28 million tons down to 500,000 tons) simply by upgrading to SCR and operating 

existing SCR controls. There is no reason to expect that emissions reductions from plants in the 

remaining states would be any less significant, indicating that coal EGU emissions as a whole 

can still be reduced by more than 3/5th with existing and widely-used control technologies. 

Table 32: Achievable Annual and Ozone Season NOx Emission Reductions from Coal 

Plants in CSAPR and New England States (2011)

Actual NOx 

(tons)

Achievable NOx 

Tons: Installation 

and Operation of 

SCR (tons)

NOx Reduction 

(Actual -

Achievable)

(tons)

NOx Reduction

Percentage (%)

Ozone season 572,724 223,179 349,545 61.0%

Annual 1,280,129 502,852 777,277 60.7%

4. Additional NOx Reductions from Coal Plants Will Have a Significant 

Ameliorative Effect on Ozone Levels 

Coal EGUs are by far the largest stationary source category of NOx emissions in the 

United States, with 2011 emissions of approximately 1.8 million tons. However, coal plants’

contributions to air quality are likely to be even more pronounced due to the coincidence of 

emissions from these plants with conditions favoring peak ozone formation. The conditions 

most conducive to the formation of ozone are also conditions that lead to increased utilization of 

the dirtiest coal EGUs: hot summer days when air conditioners are running and energy demand is 

at its highest. Coal units lacking SCR controls are often operating on these high energy demand 

days and, due to their lack of controls, can have an outsize impact on total NOx emissions and 

poor air quality. 

In order to evaluate the air quality benefits from additional, SCR-level control of the U.S. 

coal fleet, we retained Sonoma Technology, Inc. (Sonoma) to conduct air dispersion modeling 

using the Comprehensive Air Quality Model with extensions (CAMx). Sonoma used EPA’s 

2011 modeling platform, including acquiring 2011 emissions data from EPA, 2011 outputs from 

the Weather Research and Forecasting (WRF) meteorological model, and 2011 GEOS-Chem 

 

728 Installation of SCR was simulated by scaling a plant’s NOx emission rate down by the ratio of its actual average 

ozone season rate and 0.07 lb/MMBtu. The latter represents a rate that is consistent with recent entries in the 

RACT/BACT/LAER Clearinghouse and is demonstrated to be readily achievable in practice by coal units equipped 

with SCR. Indeed, according to data from EPA, during the 2013 ozone season 105 coal-fired units had NOx 

emissions at or below 0.07 lb/MMBtu. EPA, Air Markets Program Database, ampd.epa.gov/ampd/. 

729 Emissions from these sources comprise another more than 56,000 tons of 2011 NOx.
266

results to prepare initial conditions and boundary condition inputs. Emissions processing was 

conducted using the Sparse Matrix Kernel Emissions Modeling System (SMOKE). 

In order to simulate the impacts of SCR-level control of the U.S. coal fleet, Sonoma 

completed two 2011 ozone season model runs using CAMx. First, Sonoma completed a base 

case run in which EPA’s 2011 emission inventory was left unchanged. This base case run 

provided baseline hourly ozone concentrations at all 12 km x 12 km grid cells in the nationwide 

modeling domain for all hours of the 2011 ozone season. Second, Sonoma completed an SCRlevel control run in which it scaled down the emissions of coal plants in the CSAPR region to 

levels reflecting installation and operation of SCR. Using the same methodology discussed 

above in Section VII.A.3, to simulate operation of SCR for units that had already installed this 

control, each unit’s 2011 ozone season average NOx emission rate was compared to the unit’s 

best historical 30-consecutive day 24-hour emission rate (calculated using the same methodology 

described above). 2011 ozone season hourly emissions were then scaled down by the ratio of the 

best historical rate to the actual 2011 ozone season rate. This resulted in a small degree of 

scaling for most SCR units, but a larger degree of scaling for units that chronically failed to use 

or optimize use of their existing SCR. For units without SCR, the 2011 ozone season average 

NOx emission rate for each unit was scaled down by the ratio of 0.07 lb/MMBtu and the unit’s 

actual average rate to reflect the fact that any unit that installs an SCR today should be able to 

achieve an emission rate at least as good as 0.07 lb/MMBtu.

Figure 15 depicts peak 8-hour air quality improvements between the base case and SCRlevel control runs. As the figure illustrates, most areas throughout the Eastern United States 

experience peak 8-hour air quality improvements of more than 2.0 ppb; a large percentage of 

areas in the East experience peak air quality improvements of more than 3.0 ppb; and significant 

areas in many states, including Pennsylvania, West Virginia, Virginia, Ohio, Indiana, Kentucky, 

Illinois, Georgia, Alabama, Tennessee, Arkansas, Oklahoma, Texas, and Kansas experience peak 

8-hour air quality improvements of between 5.0 and 17.6 ppb. 
267

Sonoma also looked at air quality improvements in current ozone nonattainment areas 

and other major metropolitan areas. Figures 16, 17, 18 and 19 provide the results of that analysis. 

Numerous major metropolitan areas, including numerous nonattainment areas, experience large 

reductions in modeled 4th highest 8-hour daily maximum ozone concentrations as a result of 

simulated SCR-level control of the coal fleet. As shown in Figure 16, 4th highest 8-hour daily 

maximum ozone concentrations in major urban areas and nonattainment areas are reduced by as 

much as nearly 5 ppb in Cincinnati, and more than 30 major urban areas and nonattainment areas 

experiencing reductions in 4th highest 8-hour daily maximum ozone concentration of more than 1 

ppb. As shown in Figures 17, 18, and 19, the number of days during ozone season 2011 when 

modeled ozone levels exceeded key thresholds—60 ppb, 65 ppb, and 70 ppb—declined 

dramatically in many urban areas based on SCR-level control of the coal fleet. For example, 

eleven cities, including three nonattainment areas, experienced a reduction of 10 or more days 

during the ozone season when maximum 8-hour ozone concentrations exceeded 60 ppb. An 

additional 14 cities, including 11 nonattainment areas, experienced 6 or more days during the 

ozone season when maximum 8-hour ozone concentrations exceeded 60 ppb. 

Reductions in exceedances of 65 and 70 ppb were also widespread in the SCR-level 

control run. Four metropolitan areas, including two nonattainment areas experienced a reduction 

of 10 more days during the ozone season when maximum 8-hour ozone concentrations exceeded 

65 ppb. An additional 15 metro areas, including seven nonattainment areas, experienced 6 or 

more days during the ozone season when maximum 8-hour ozone concentrations exceeded 65 
268

ppb. And 19 metro areas, including five nonattainment areas, experienced 4 or more days during 

the ozone season when maximum 8-hour ozone concentrations exceeded 70 ppb. 

Figure 17

Figure 18
269

Figure 19
270

Figure 20

5. Tremendous NOx Reductions--from Coal Fired EGUs as well as from 

Other Sources--Can Be Achieved Cost-Effectively And Have Been 

Judged to Be Economically Reasonable Time and Again 
271

Not only are significant additional NOx and VOC reductions available, but they can be 

achieved at a reasonable cost, far below recent industry estimates, which have repeatedly proven 

to be significantly exaggerated. 

NOx is a precursor for ozone that originates from a wide variety of stationary and mobile 

sources. The vast majority of NOx comes from anthropogenic sources. According to data from 

EPA’s National Emissions Inventory (NEI), the top U.S. sources of NOx are dominated by onroad light- and heavy-duty vehicles and coal-fired power generation. 730 For these and other 

categories, there are many cost-effective methods readily available for reducing NOx pollution.

Again, some of the most cost-effective reductions are achievable from the nation’s coalfired EGUs. Coal-fired power plants are the third largest source category of NOx emissions, 

emitting 11.5% of NOx nationwide. They are also the largest type of stationary source by a 

significant margin, emitting over twice as much NOx per year as the second largest stationary 

source category, natural gas-fired industrial boilers and internal combustion engines (ICEs). As 

discussed in Section VII.A above, simply ensuring that power plants that have already upgraded 

their emission controls actually operate them consistent with best demonstrated historical rates 

has the potential to reduce total coal EGU emissions by approximately 1/6th. Dr. Sahu in his 

analysis not only quantified the emission reductions achievable both annually and during the 

ozone season from coal plants with SCRs already installed fully operating these controls, but he 

also quantified the cost per ton of doing so. As detailed in Dr. Sahu’s accompanying report, Dr. 

Sahu relied on industry estimates of variable operating and maintenance costs for additional 

reagent use and catalyst replacement and disposal developed by Sargent and Lundy for EPA’s 

Integrated Planning Model.731 Dr. Sahu concluded that by simply running already installed 

controls at proven levels it is possible to achieve 136,534 tons of additional ozone season NOx 

emission reductions each year at a total cost of $63.5 million and a cost/ton of only $465. And it 

is possible to achieve 296,160 tons of additional annual NOx reductions each year at a total cost 

of $129.5 million and a cost/ton of just $437. 

Beyond these extremely cost-effective NOx reductions from simply operating installed 

controls, there are significant additional highly cost-effective reductions from the more poorly 

controlled remainder of the coal fleet. Control measures for coal-fired EGUs are low-hanging 

fruit offering cost-effective NOx reductions. EPA has determined that “there likely would be 

very large emissions reductions available from EGUs before costs reach the point for which nonEGU sources have available reductions.”732 By installing and operating SCR in combination with 

low-NOx burners (LNB) and over-fired air (OFA), existing plants can remove NOx at rates 

between $1,210 and $4,550 (2015$) and up to 89% control efficiency.733 SCR plus sorbent 

 

730 U.S. EPA NEI version 2, available at http://www.epa.gov/ttnchie1/net/2011inventory.html (accessed Mar. 9, 

2015).

731 Sargent and Lundy, IPM Model – Updates to Cost and Performance for APC Technologies SCR Cost 

Development Methodology Final March 2013, available at (see also Exhibit 29, Exhibit 30, Exhibit 31) 

http://www.epa.gov/airmarkets/documents/ipm/attachment5_3.pdf. (See Exhibit 28). 

732 76 Fed. Reg. 48208, 48249 (Aug. 2, 2011)

733 See e.g., Technical Support Document to Comments of Conservation Organizations, Proposed Federal 

Implementation Plan To Address Regional Haze Requirements for the Navajo Generating Station Units 1, 2 and 3 

(Dec. 30, 2013); 77 Fed. Reg. 50,936 (Aug. 23, 2012); 78 Fed. Reg. 8,273–8,294 (Feb. 5, 2013); Enviroplan 

Consulting, Final Findings Report Golden Valley Electric Association (GVEA) Best Available Retrofit Technology 
272

injection has control costs of $1,690 to $2,060 (2015$).734 For SCR alone, existing coal EGUs 

control costs range from $2,835 to $3,430 (2015$).735 

Significant cost-effective emission reductions are also available from mobile sources. 

According to EPA, most controls for mobile sources can be installed and operated at between 

$1,160 and $5,500 (2015$)736 per ton of NOx or NOx+non-methane hydrocarbons, with average 

costs ranging from $3,500 to $7,000.737 Moreover, many measures produce fuel savings, 

offsetting control costs and even resulting in net savings in some cases. 

On-road diesel heavy-duty vehicles are responsible for over 19% of U.S. NOx 

emissions.738 Retrofitting diesel vehicles with cleaner equipment – such as installation of SCR -

can be performed at costs as low as $4,966 (2015$) per ton for class 8 vehicles.739 Retrofits of 

class 6 and 7 heavy duty vehicles and commuter programs are also available, though they have 

higher costs per ton in part because they do not necessarily provide large emission reductions.740

Technology to reduce long idling on heavy-duty diesel vehicles can reduce NOx and actually 

save money by reducing fuel costs.741 For example, two measures to eliminate idling on heavyduty diesel vehicles, such as advanced truck electrification--which provide trucks parked 

overnight with electrical power, heating, and cooling to avoid running the engines--and installing 

truck auxiliary power units--a small engine and generator that provides power to the truck with 

the main engine shut off--cost between $1,600 to $3,950 (2015$) per ton of NOx and VOC.742

These measures are in various stages of build out in a number of states. Off-road diesel vehicles 

are also major NOx emitters, and are accompanied by a range of control costs, starting at around 

$2,120 for engine upgrades.743

For light-duty vehicles, which emit 16.5% of U.S. NOx, median costs for operating 

continuous inspection and maintenance programs are around $2,550 per ton of NOx and VOCs, 

although these programs, too, can actually pay for themselves and in fact save money in the 

 

(BART) Evaluation (April 27, 2009); 77 Fed. Reg. 76,871 (Dec. 31, 2012); 77 Fed. Reg. 76,871 (Dec. 31, 2012); 77 

Fed. Reg. 72,511 (Dec. 5, 2012); 77 Fed. Reg. 72,511 (Dec. 5, 2012); U.S. EPA, RACT/BACT/LAER 

Clearinghouse, available at http://cfpub.epa.gov/RBLC; 77 Fed. Reg. 40,151 (July 6, 2012).

734 See e.g., 76 Fed. Reg. 52,388 (Aug. 22, 2011).

735 See e.g., 75 Fed. Reg. 64,221 (Oct. 19, 2010); 77 Fed. Reg. 51,915 (Aug. 28, 2012); 76 Fed. Reg. 80,754 (Dec. 

27, 2011); 75 Fed. Reg. 64,221 (Oct. 19, 2010).. 

736 All costs converted to 2015 $ using the CPI inflation calculator. http://data.bls.gov/cgi-bin/cpicalc.pl. 

737 U.S. EPA, Chapter 3: Emissions Controls Analysis –Design and Analytical Result, Final Regulatory Impact 

Analysis (RIA) for the NO2 National Ambient Air Quality Standards (NAAQS) (Jan. 2010), available at

http://www.epa.gov/ttnecas1/regdata/RIAs/FinalNO2RIACh31-20-10.pdf.

738 See National Emissions Inventory, 2011.

739 U.S. EPA, Menu of Control Measures. Last updated April 2012, available at

http://www.epa.gov/air/criteria.html; U.S. EPA, Update of the Control Measures Database for Onroad Sources with 

MOVES, OAQPS (Contract No. EP-D-07-097, WA No. 4-09). Prepared by TranSystems (2011). 

740 U.S. EPA, Chapter 3, supra note 725.

741 U.S. EPA 2012, Menu of Control Measures supra note 727; U.S. EPA, 2011: "Update of the Control Measures 

Database for Onroad Sources with MOVES". Prepared for the U.S. Environmental Protection Agency, OAQPS; 

http://www.epa.gov/ttnecas1/regdata/RIAs/FinalNO2RIACh31-20-10.pdf

742 Per ton NOx and VOCs. Cost-effectiveness uses weighting ratio of 4:1 for NOx:VOC; U.S. EPA, The CostEffectiveness of Heavy-Duty Diesel Retrofits and Other Mobile Source Emission Reduction Projects and Programs, 

Transportation and Regional Programs Division Office of Transportation and Air Quality(May 2007).

743 U.S. EPA. Lists of Potential Control Measures for PM 2.5 and Precursors (2007).
273

long-run.744 Commuter programs offer incentives to reduce light-duty vehicle miles traveled and 

trips, with programs such as regional rideshares, vanpool programs, park-and-ride lots, regional 

transportation demand management, and employer trip reduction program. EPA reports that the 

costs for operating these programs start as low as $1,630 (2015$) per ton of NOx and VOCs745, 

with median costs across all types of commuter programs running at $26,000 per ton.746 On 

average, EPA has estimated that implementing more stringent requirements for aftermarket 

replacement catalytic converters could reduce NOx at a cost of $3,700 per ton. 747

Simply retiring dirty vehicles can be a cost effective measure for reducing NOx pollution. 

Vehicle retirement programs for heavy-duty diesel vehicles can be cost-effective, as has been 

demonstrated by California’s Carl Moyer Grant Program, which performed retirements at an 

overall cost of $3,040 (2015$) per ton.748 California’s Bay Area Air Quality Management 

District’s retirement program estimated cost-effectiveness at $7,000 to $8,115 (2015$) per ton 

and was funded by a $4 increase in car registration fees.749,750

Many low cost reductions have already been made available through EPA’s national 

vehicle standard. EPA programs tightening emissions standards for both on-road and non-road 

mobile sources and reducing the sulfur content of gasoline and on- and non-road diesel fuel, 

along with fleet turnover, have already caused mobile NOx emissions to begin to decline 

significantly.751 EPA’s Tier 3 Motor Vehicle Emission and Fuel Standards, which come into 

effect in 2017, are projected to reduce NOx at a cost of $4,484 a ton by 2030.752

Cost-effective NOx reduction measures are within reach. While EPA ultimately must set 

the primary standard at a level that protects public health, without consideration of cost, 

affordable application of existing technology can offer NOx reductions from major sources at a 

reasonable cost. 

B. The Benefits of a 60 ppb Ozone Standard Outweigh the Costs

 

744 *Per ton NOx and VOC. Cost-effectiveness uses weighting ratio of 4:1 for NOx:VOC. 

U.S. EPA. The Cost-Effectiveness of Heavy-Duty Diesel Retrofits and Other Mobile Source Emission Reduction 

Projects and Programs. Transportation and Regional Programs Division Office of Transportation and Air Quality. 

May 2007.; http://www.epa.gov/ttnecas1/regdata/RIAs/FinalNO2RIACh31-20-10.pdf

745 1:4 weighted sum of VOC and NOx

746 http://www.epa.gov/ttnecas1/regdata/RIAs/452_R_08_003.pdf

747 http://www.epa.gov/ttnecas1/regdata/RIAs/FinalNO2RIACh31-20-10.pdf

748 Wagner and Rutherford. Survey of Best Practices in Emission Control of In-Use Heavy-Duty Diesel Vehicles. 

ICCT. CCAC. August 2013.

749 http://www.nj.gov/dep/baqp/rapt/wps/DI009_fin.pdf

750 As a higher-end example for light-duty vehicles, costs for a small-scale vehicle retirement programs in Illinois 

ran around $76,350 a ton of NOx (2015$). See http://escholarship.org/uc/item/1h30m2r7. The National Association 

of Manufactures (NAM) has recently estimated the cost per ton of reducing NOx via “Cash for Clunkers” at a 

whopping $500,000 per ton. See - http://www.nam.org/Issues/Environment/Ozone-Regulations/NERA-NAMOzone-Full-Report-20140726.pdf. The 2009 “Cash for Clunkers” program was designed as an economic stimulus 

program, never as a cost-effective NOx reductions strategy. Even the high cost of $76,350 cited here is still seven 

times lower than NAM’s baseless estimate used in analyses regarding the compliance costs of the new ozone 

NAAQS. See discussion in Section VII.B, below. 

751 U.S.EPA. Non-EGU Emissions Reductions Cost and Potential. Technical Support Document (TSD) for the 

Transport Rule. Docket ID No. EPA-HQ-OAR-2009-0491. Office of Air and Radiation. May 2010.

752 U.S. EPA. Draft Regulatory Impact Analysis: Tier 3 Motor Vehicle Emission and Fuel Standards. March 2013.
274

Though, as explained in Section VII.A above, the cost-benefit balance is not relevant and 

EPA must not consider it, if it were relevant, it would strongly favor a 60 ppb ozone standard. By 

EPA’s own calculation, for the states outside of California, the net benefits—even accounting for 

compliance costs—of setting the ozone standard level to 60 ppb is approximately $13 billion. 

And as EPA has recognized, compliance cost estimates often exceed actual costs in practice.753 

Many of the emission reductions required to achieve a lower ozone standard have already 

been baked into final and proposed rules. As discussed above in Section VII.A, these rules will 

significantly ratchet down emissions of ozone precursors, dramatically reducing the cost of 

compliance with a new, lower ozone standard. As the Office of Management and Budget’s 

(OMB) Office of Information and Regulatory Affairs recently confirmed, it is not appropriate to 

double count the costs associated with those rules in estimating the cost of compliance with a 

new ozone NAAQS.754 Consistent with this principle, OMB excluded the benefits and costs 

associated with the 2006 PM2.5 NAAQS from its 10-year aggregate and year-by-year estimates 

to prevent double-counting due to implementation of CSAPR.755 The NOx reduction co-benefits 

of the soon to be finalized Clean Power Plant will also reduce the cost of compliance with a new 

ozone standard.

As EPA well knows, industry has a consistent track record of grossly overstating the 

costs of proposed new rules.756 Industry always argues that new regulations will be 

tremendously expensive and harm the economy, but industry’s assertions have proven false. For 

example, in 1990, when strengthening amendments to the Clean Air Act were proposed, utilities 

forecasted that reducing sulfur dioxide would cost $1,000 to $15,000 per ton and that electric 

rates would increase by 10%.757 In reality, the reductions cost only $100-$200 per ton, 5-75 

times less than what industry predicted.758 At the same time electric rates fell in most states. 

The latest effort to impermissibly inject cost considerations into the NAAQS-setting 

process for ozone is no different. The NERA Economic Consulting analysis completed on 

 

753 U.S. EPA, Regulatory Impact Analysis, 8-11 (2014) (finding “[s]tudies indicate that it is not uncommon for preregulatory cost estimates to be higher than later estimates, in part because of difficulty in predicting technological 

changes”).

754 White House Office of Management and Budget, Office of Information and Regulatory Affairs. 2014 Draft 

Report on the Benefits and Costs of Federal Regulations and Unfunded Mandates on State, Local, and Tribal 

Entities. (2014), at 14.

755 See id.

756 EPA Admin’r Lisa P. Jackson, Remarks on the 40th Anniversary of the Clean Air Act, As Prepared, 

yosemite.epa.gov/opa/admpress.nsf/12a744ff56dbff8585257590004750b6/7769a6b1f0a5bc9a8525779e005ade13!O

penDocument (Sept. 14, 2010) (“Today’s forecasts of economic doom are nearly identical—almost word for word—

to the doomsday predictions of the last 40 years. This ‘broken-record’ continues despite the fact that history has 

proven the doomsayers wrong again and again.”).

757 U.S. House of Representatives, Committee on Energy and Commerce, Democratic Staff, The Clean Air Act’s 

Track Record: Cleaner Air and Economic Growth (2013), available at 

http://democrats.energycommerce.house.gov/sites/default/files/documents/Fact-Sheet-The-Clean-Air-Act-2013-6-

25.pdf.

758 Id; see also U.S. House of Representatives Committee on Energy and Commerce, Industry Claims about the 

Costs of the Clean Air Act (2009), available at: 

http://democrats.energycommerce.house.gov/Press_111/20090616/dc_industryjobs.pdf. 
275

behalf of the National Association of Manufacturers (NAM)759 both wholly disregards the 

myriad public health benefits associated with a more health-protective NAAQS and attendant 

avoided medical expenses associated with asthma-induced emergency department visits, asthma 

hospitalizations, and missed work and school days. Moreover, it also massively distorts the cost 

of compliance by basing all NOx reductions of unknown origin on an assumed cost/ton of 

$500,000. 

The NAM study authors have admitted that the huge difference between their asserted 

$500,000 per ton compliance cost for unknown controls and EPA’s far lower estimates, is due 

“almost entirely” to a cost methodology that is based upon the “Cash for Clunkers” economic 

stimulus program.760 Cash for Clunkers was not a program intended to drive NOx reductions: it 

was a program that was intended to drive the purchase of new vehicles. Any NOx reductions 

were incidental benefits. Independent, academic experts have characterized this NAM cost 

methodology as “insane” and “unmoored from economic reality.” 761 As discussed above, 

NAM’s cost estimates are well over 1,000 times higher than the cost at which 1/6th of U.S. coal 

plant emissions could be reduced. It is approximately 100 or more times higher than the cost/ton 

at which SCR can and has been added to many coal plants. And it is orders of magnitude higher 

than the cost-effective emission reductions from the mobile source sector discussed above.

In 2011, EPA reviewed the costs and benefits of the steps taken under the Clean Air Act 

authority from 1990 to 2010 and projected to 2020. In a peer-reviewed study, they found that by 

2020, the benefits of Clean Air Act will have outweighed the costs by 30:1.

762

 Congress receives 

an annual report from the White House on the costs and benefits of federal programs. Under both 

Republican and Democratic Administrations, benefits have always been much higher than costs. 

Looking at the decade from 2002 to 2012, the OMB calculated the benefits of 21 EPA air 

pollution rules at up to $529.1 billion, compared to $35.3 billion in costs (in 2001 dollars).763

According to EPA, since 1970 industry and other regulated parties have been able to cut 

harmful air pollution by approximately seventy percent (70%) while the economy has grown by 

tripled. Since 1980, ozone levels have been reduced by thirty-three percent (33%) across the 

 

759 NERA Economic Consulting, Assessing Economic Impacts of a Stricter National Ambient Air Quality Standard 

for Ozone, (July 2014) (Note: this report predated EPA’s proposal by five months, and made numerous assumptions 

where information was unavailable) available at http://www.nam.org/Issues/Environment/OzoneRegulations/NERA-NAM-Ozone-Full-Report-20140726.pdf

760 See “Industry Report Identifies Higher Costs For Ozone Proposal Than EPA Estimates,” Bloomberg BNA Daily 

Environment Report (Feb. 27, 2015) (Attachment __).

761 See “Experts: Pro-Smog Pollution Report Is ‘Unmoored From Reality,’ 

http://mediamatters.org/research/2014/08/20/experts-pro-smog-pollution-report-is-unmoored-f/200490 (Aug. 20, 

2014) (quoting Professor Michael Livermore, senior advisor at New York University's (NYU) Institute for Policy 

Integrity) (emphasis added) (Attachment __). For a thorough critique of the multitude of flaws and biases in the 

NAM cost study, see generally id. and “National Association of Manufacturers: Thin Air,” Laurie Johnson, 

http://switchboard.nrdc.org/blogs/ljohnson/national_association_of_manufa.html (Sept. 16, 2014) (Attachment __).

763 Executive Office of the President, Office of Management and Budget. 2013 Report to Congress on the Benefits 

and Costs of Federal Regulations and Unfunded Mandates on State, Local. And Tribal Entities. March, 2014. 

Available at http://www.whitehouse.gov/sites/default/files/omb/inforeg/2013_cb/2013_cost_benefit_reportupdated.pdf. 
276

country. For over 45 years, there has been little to no evidence of economic damage due to the 

abatement of air pollution.

C. The Phenomenon of NOx Scavenging Does Not Counsel a Higher Ozone 

Standard 

Industry and other petitioners have sought to use the “ozone scavenging” phenomenon –

whereby fresh NOX emissions at ground level can “scavenge” ozone molecules and reduce ozone 

concentrations measured by surface monitors – as an argument against setting a lower ozone 

standard. According to these petitioners, lowering the ozone standard would require increasing 

relative NOX concentrations, which, in turn, would lower the rate of ozone scavenging and 

therefore increase ozone levels in urban cores, where fresh NO emissions are typically found. 

This argument rests on multiple assumptions: (1) that ozone destruction is simply a function of 

increased NOX levels in VOC-limited areas, (2) that ozone scavenging is an effective pollution 

control mechanism, and (3) that the increased strategic NOX reductions accompanying a lower 

ozone NAAQS will result in harmful ozone increases in all urban cores. As shown below, these 

assumptions are false.

This is fundamentally an argument based on control considerations; as such, it is not 

legally relevant for the reasons discussed above in Section VII.A. Even if considered (which it 

should not be), the ozone scavenging argument against lowering ozone NAAQS should be 

rejected because it rests on an incomplete understanding of both the science of ozone formation 

and EPA modeling. More importantly, it should be rejected because, contrary to what its 

opponents claim, a lower ozone standard will result in significant health benefits for urban cores 

populations.

1. Ozone Formation is Complex and Non-Linear

The formation of ozone is a complex process involving nonlinear change in response to 

hundreds of precursors.764 In particular, NOX precursors can lead to both the formation and the 

destruction of ozone, depending on the local concentrations of NOX, VOC, and radicals such as 

the hydroxyl (OH) and hydroperoxy (HO2) radicals, as well as local meteorological 

conditions.765 NOX emissions contribute to ozone formation in so-called “NOX-limited” areas, 

which feature high VOC/NOX ratios, where the production of ozone varies directly with NOX

concentrations (e.g., downwind of important NOX sources, typically in rural or suburban areas). 

NOX contributes to ozone destruction in so-called “VOC-limited” areas,766 which feature low 

VOC/NOX ratios, where ozone ozone is destroyed through NOx scavenging767 (e.g. in downtown 

metropolitan areas, close to busy streets and roads, and in power plant fumes). However, while 

 

764 California Air Resources Board, The Physics and Chemistry of Ozone, Section 1.1. Available at: 

http://www.fraqmd.org/ozonechemistry.htm.

765 DRAFT RULE, at 75242; HREA, at 2-5.

766 Also called “radical limited” or “NOx-saturated.” California Air Resources Board, The Ozone Weekend Effect in 

California, Staff Report, at 20 (June 30, 2003). Available at http://www.arb.ca.gov/research/weekendeffect/arbfinal/web-executive-summary.pdf (hereinafter, “CARB Staff Report”).

767 NOX scavenging refers to the process whereby O3 is depleted by reaction with NO to form NO2. Also referred to 

as “ozone titration.” 
277

NOX can “destroy” ozone through titration in the immediate vicinity of emission sources, the 

resulting NO2 will later lead to ozone formation downwind. 

Though the VOC/NOX-limited paradigm is often used to explain ozone formation, the 

relationship between ozone and its precursors “is actually much more complicated than implied 

by the simple description of VOC-limited v. NOX-limited conditions.”768 Generalizations about 

the impact of control strategies on the amount of ozone in an area are therefore “difficult to make 

because of the fact that the relationship depends strongly on local conditions such as topography, 

and spatial distributions and types of emission sources, which vary from one city to another, and 

on meteorological conditions that vary from day-to-day” (noting that the interplay between NOx 

and VOC is affected by their ratio, the reactivity of the VOC mix, the role of biogenic 

hydrocarbons, the extent of photochemical aging; and the severity of an air pollution event).769

Indeed, the VOC-limited and NOX-limited labels do not neatly correspond to the urban/rural 

divide: some cities are strongly or primarily VOC-limited (e.g. Los Angeles, San Francisco, 

Phoenix, New York), others have mixed VOC-NOx-limitations (e.g. Houston, Philadelphia), and 

still others are NOX-limited (e.g., Atlanta, Nashville).770 Finally, the VOC- NOX-limited 

explanation is incomplete, as there are other chemical processes partially contributing to or 

causing ozone destruction in VOC-limited areas.771

Accordingly, ozone response to NOX emissions reductions is complex and may include 

ozone decreases at some times and locations and ozone increases in other times and locations.772

Generally, in NOX-limited conditions, ozone concentrations are most effectively reduced by 

lowering NOX rather than VOC emissions, while the reverse is true in VOC-limited conditions. 

However, a VOC-only reduction strategy is not robust enough to achieve desired ozone 

reductions in most VOC-limited areas, and further, even in VOC-limited areas, “very large 

decreases in NOx emissions can cause the O3 formation regime to become NOX-limited. 

Consequently, reductions in NOX emissions (when large), can make further emissions reductions 

more effective at reducing O3.”773 Additionally, not all areas fall neatly into either a NOX-limited 

or a VOC-limited category, both because there is a transitional region, where ozone is less 

sensitive to marginal changes in either NOX or VOCs774 and because the NOX-VOC ratio of a 

certain area can vary significantly from day to day.775 Accordingly, “the key question is whether 

controlling NOX is beneficial or counterproductive for an area as a whole, not just at a single 

 

768 U.S. Congress, Office of Technology Assessment, (July 1989). Catching Our Breath: Next Steps for Reducing 

Urban Ozone, at 99 (hereinafter, “OTA Report”)

769 OTA Report, at 97; see also Sillman, S., Overview: Tropospheric Ozone, Smog and Ozone-NOx-VOC Sensitivity.

Available at: http://www-personal.umich.edu/~sillman/ozone.htm#OZO1.2.1.

770 See Duncan B., et al. (2009). The Sensitivity of U.S. Surface Ozone Formation to NOx and VOCs as Viewed 

From Space, at 3-4. Available at 

https://www.cmascenter.org/conference/2009/abstracts/duncan_sensitivity_us_2009.pdf (hereinafter, “2009 

Duncan”); see also ISA, at 3-7.

771 CARB Staff Report, at 17 (suggesting “NOx reductions, different timing of emissions including NOx, different 

amounts and impacts of pollutants that persist overnight aloft, different amounts of light-absorbing particulate matter 

in the air, and ozone quenching by nitric oxide emissions” as equally plausible explanations for the weekend effect).

772 HREA, Section 2.2.1.

773 HREA, at 2-5. 

774 HREA, at 2-5. 

775 OTA Report, at 102.
278

location.”776

2. Ozone Scavenging Is Not A Pollution Control Mechanism – It Is A 

Pollution-Moving Mechanism 

Arguing that the EPA should not set a lower ozone standard because doing so would 

reduce NOX scavenging in urban cores assumes that NOX scavenging is an effective and 

acceptable pollution control mechanism. It is neither. NOX scavenging is not a solution to the 

problem of ozone formation, because while “NOx can initially destroy O3 near the emission 

sources, these same NOX emissions eventually do react to form more O3 downwind.”777 In other 

words, NOX scavenging does not actually destroy ozone, it merely delays its formation, and 

shifts it downwind. NOX scavenging is also an unacceptable pollution control mechanism 

because it results in the creation of NO2, which is another harmful criteria pollutant. Finally, 

NOX scavenging does not address the problem of NOX itself, which is a key precursor not only 

of ozone, but also of particulate matter (PM) and other compounds with health and 

environmental concerns.778 Therefore, reducing NOX emissions is beneficial not only because it 

is necessary to meet a lower O3 standard, but also because it will result in health benefits beyond 

those directly associated with reducing ambient O3 concentrations.779

3. Even If Scavenging Were Relevant, Lowering the Ozone Standard 

Will Produce Health Benefits In All Areas, Including Urban Cores

a. The Ozone Scavenging Implications of Reduced NOX

Emissions Are Extremely Limited 

The ozone scavenging implications of NOX emissions reductions accompanying lower 

standards is extremely limited, both temporally and geographically. As the EPA’s photochemical 

model simulation in the current revision of ozone NAAQS shows, adjusting NOX emissions 

reductions to meet existing and alternative standards resulted in an overall narrowing of the 

range of ozone concentrations: as peak ozone concentrations (typically occurring in rural or 

suburban areas, during warm months, on days with higher ozone concentration) tended to 

decrease, concentrations in the lower part of the ozone distribution (typically occurring in urban 

areas, including urban cores, during cool months, on days with lower ozone concentration) 

tended to increase.780 Additionally, NOX emissions reductions accompanying lower ozone

standards generally decreased ozone concentrations in the high and mid-range portions of the 

ozone distribution in rural, urban and suburban areas, as well as most urban cores.781

Further, the ozone scavenging implications of NOX emissions reductions in urban cores 

was extremely restricted: NOx reductions in urban cores generally decreased peak concentrations 

 

776 OTA Report, at 102.

777DRAFT RULE, at 75242.

778 These include nitrogen dioxide (NO2), nitric acid (HNO3), nitrous acid (HONO), peroxyacetylnitrate (PAN), 

nitro-polycyclic aromatic hydrocarbons (nitro-PAHs), regional haze, and nitrate deposition with subsequent 

fertilization and eutrophication of soils and surface waters. CARB Staff Report, at 20.

779 DRAFT RULE, at 75285; CARB Staff Report, at 8.

780 HREA, Sections 4.3.3.2 (Figures 4-9 and 4-10) and 9-7 and at 8-48; DRAFT RULE, at 75242.

781 HREA, at 9-7.
279

and increased lower concentrations (as they did in the larger study areas) but they only increased 

concentrations near the center of the ozone distribution in a small subset of cities. Ozone 

responses near the center of the ozone distribution in urban cores followed one of the three 

patterns shown in the following table:

HREA, at 9-7 (Table 9-3). As Table 9-3 shows, no seasonal mean increases were found in the 

majority of the cities studied (Atlanta, Sacramento, Washington D.C., Baltimore, Cleveland, 

Dallas, Detroit, Los Angeles, New York, Philadelphia, and St. Louis) at any of the proposed 

alternative standards, while increases in mean seasonal ozone at alternative standards were only 

found in four cities (Boston, Chicago, Denver and Houston).782 Additionally, the extent and 

impact of any such ozone increases was further mitigated by the fact that increases were slight 

and occurred mostly on days with lower ozone concentrations, such as “during cool, cloudy 

weather and at night when photochemical activity is limited or nonexistent.”783 Accordingly, 

while reductions in NOX precursors led to increases in ozone in certain locations, those increases 

were restricted to the middle and lower ends of the ozone distribution and a small number of 

urban cores, and they did not get progressively larger as alternative standards were lowered. 

b. Any Health Risk Increases Resulting From Reduced Ozone 

Scavenging Are Limited at 70 ppb and Offset Entirely at 60 

ppb

Ozone increases resulting from reduced ozone scavenging in urban cores do not translate 

into significant health risk increases. To begin with, urban core populations would be expected to 

experience important reductions in both ozone exposures and ozone -induced lung function risks 

when meeting alternate standards.784 Further, while urban core areas “in some cases show[] 

overall increases in epidemiology-based mortality and morbidity risk”, these increases are not 

substantial: only 3 of the 12 urban study areas (Boston, Detroit, and Houston) exhibited an 

increase in the percentage change in ozone-attributable risk after meeting the 70 ppb standard 

 

782 HREA, at 9-7 (Table 9-3).

783 DRAFT RULE, at 75242; see also HREA, at 7-55—7-56 (Figures 7-2 and 7-3) (showing that increases in O3

(and resulting estimated increases in risk) occur largely on days with initial O3 concentrations in the range of 10 to 

40 ppb).

784 HREA, at 9-42 (emphasis added).
280

(compared to risk that meets the current standard) and only did so in the 2009 simulation year.785

Importantly, those increased risks are offset entirely when adjusted to meet the lowest alternative 

standard (60 ppb).786 Id. Furthermore, even those increases are likely to be mitigated through a 

concurrent VOCs/ NOX reduction strategy. See infra, Section VII.C.3.iii.

c. The Effects of Reduced Ozone Scavenging Can Be Mitigated 

With a Combined VOCs/NOx Reduction Strategy

In assessing the ozone air quality response to reducing both NOX and VOC emissions for 

a subset of seven urban study areas, the EPA found that a concurrent VOCs/NOx reduction 

strategy mitigates median ozone level increases.787 Specifically, the addition of VOC reductions 

generally resulted in larger decreases in mid-range ozone concentrations (25th to 75th 

percentiles), and reduced the low concentration ozone increases in all seven of the urban study 

areas evaluated.788 Given that the EPA’s reduction strategies and broad nationwide emission cuts 

are merely crude approximations of the actual strategies individual states can pursue, it is more 

than likely that state implementation plans will be even more efficient at mitigating the effects of 

O3 scavenging. 

Indeed, there is a long success record for concurrent reductions of VOCs and NOX. NOX

scavenging is not a new phenomenon – also referred to as “the weekend effect”, it has been a 

part of pollution control strategies for decades. CARB, facing the highest ozone levels and the 

most VOC-limited urban area in the country, has been pursuing a strategy of concurrent VOCs 

and NOX reductions for more than thirty-five years, and has been successful at reducing the high 

ozone levels all over southern California.789 While acknowledging temporary ozone increases 

through reduced NOx scavenging, CARB maintains that “NOX reductions are not counterproductive for attaining ambient air quality standards” and that “ozone air quality has improved 

most when NOX air quality has also improved.”790 In other words, NOX scavenging demands an 

optimized reduction strategy, not a higher ozone standard.

VIII. CONCLUSION

For all of the reasons explained above, EPA should heed its duty to follow the science 

and establish the ozone NAAQS at a level that is truly protective of public health with and 

adequate margin of safety: 60 parts per billion. 

Respectfully submitted,

Janice Nolan, Assistant Vice President, National Policy

 

785 HREA, at 7-69 (Table 7-7 and 7-8).

786 The risk is increased in simulating estimated risk from moving from recent conditions to just meeting the existing 

standard. See HREA, Appendix 7b, Tables 7B-1 and 7B-2 (showing increases for Houston and Los Angeles for the 

2007 year, and increases for Boston, Cleveland, Houston, Los Angeles, New York, Philadelphia for the 2009 year). 

787 DRAFT RULE, at 75278.

788 DRAFT RULE, at 75278 (citing HREA, Appendix 4D, Section 4.7).

789 CARB Staff Report, at 6.

790 CARB Staff Report, at 9.
281

American Lung Association

Deborah Shprentz

Consultant to the American Lung Association

Georgia Murray, Staff Scientist

Appalachian Mountain Club

Kevin Bundy, Senior Attorney

Anna “Mickey” Moritz, Legal Fellow

Center for Biological Diversity

Joseph O. Minott, Esq., Executive Director

Ryan Knapick, Staff Attorney

Clean Air Council

David Baron

Seth Johnson

Attorneys

Earthjustice

Elena Craft, PhD, Senior Health Scientist

Environmental Defense Fund

Stephanie Kodish, Director & Counsel, Clean Air Program

National Parks Conservation Association

John Walke, Clean Air Director

Emily Davis, Staff Attorney

Natural Resources Defense Council

Josh Stebbins, Managing Attorney

Josh Berman, Staff Attorney

Sierra Club
282

Appendix of Additional Comments of Members of the Clean Air Scientific Advisory 

Committee

Dr. John Balmes, a clinician, pointed to critical controlled human exposure studies and a 

reanalysis of the Adams 2006 study published subsequent to the 2008 review, and now 

considered in the current review. 

“Since the scientific evidence was reviewed for the preparation of the 2006 Criteria 

Document for Ozone, the results of the Adams et al. (2006) study have been carefully 

reanalyzed (Brown et al., 2008) and actually show a statistically significant group effect. 

In addition, two other studies have shown statistically significant decrements in FEV1 

after 6.6-hour exposures to 0.070 ppm (Schelgele et al., 2009) and 0.060 ppm (Kim et al., 

2011), respectively.” 

Dr. Balmes also referenced newly published studies that are now part of the record of this 

review. 

“The reanalysis shows a statistically significant group decline in FEV1 at 60 ppb in the 

Adams study, at 70 ppb in the Schelgele study, and at 60 ppb in the Kim study, after 6.6 

hour exposures. These findings only reinforce the need for a standard of 60 ppb.” 

He further explains the clinical significance of a ten percent decrement in FEV1, and the fact that 

in the absence of a threshold, even a standard of 60 ppb would not be fully protective of all 

individuals. 

“From a clinical perspective, a 10% decrement in FEV1 is often associated with 

respiratory symptoms, especially in individuals with pre-existing pulmonary or cardiac 

disease. For example, people with chronic obstructive pulmonary disease have decreased 

ventilatory reserve (i.e., decreased baseline FEV1) such that a ≥ 10% decrement could be 

associated with moderate to severe respiratory symptoms. From a public health 

perspective, the exposure and risk assessment conducted for the last review of the ozone 

NAAQS clearly document that a substantial proportion of the U.S. population is exposed 

to levels of ozone at the various alternative standards considered. This means that even if 

a NAAQS of 0.060 ppm were to be selected, some sensitive individuals could still be 

exposed to concentrations that could cause them to have a clinically relevant decrement 

in lung function”.

“The cumulative evidence to date on the ozone exposure-lung function response 

relationship strongly suggests that it is linear with no threshold, at least through 0.060 

ppm. Therefore, it is reasonable to assume a similar exposure-response relationship for 

exacerbations of asthma. Considering the patterns of change in the estimates of 

exposures at alternative standards, as well as the uncertainties and limitations of the 

estimates, it is likely that susceptible individuals would still be adversely affected at a 
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NAAQS of 0.060 ppm, although the number of such individuals would be substantially 

lower than at higher alternate standards.”

Commenters urge EPA to heed this advice and to set a standard at the most protective level now 

under consideration, that is 60 ppb. Committee member Dr. Joe Brain cited the importance of 

inflammatory responses: 

“Chronic inflammation and the presence of increased neutrophils and neutrophil 

elastase raise concerns. Chronic inflammation and resulting increased levels of reactive 

oxygen species (ROS) may result in cumulative irreversible damage. These changes raise 

concerns about increases in morbidity and mortality caused by chronic exposure to 

ozone.”

Dr. Brain’s comment is relevant to the Kim et al 2011 study that found inflammation after 6.6 

hour exposures to 60 ppb. 

Dr. James Gauderman commented on the statistical soundness of the Brown 2007 reanalysis. 

“In the re-analysis of Adams (2006) study of 30 subjects by EPA (Brown, 2007), a small 

but statistically significant decline in FEV1 was observed. Specifically, a 2.85% mean 

O3-induced decline in FEV1 was observed following 6.6 hr square wave exposure to 

0.060 ppm O3 compared to 6.6 hr filtered air (FA) exposure. The statistical analysis by 

EPA was based on a straightforward paired comparison, and they conservatively used a 

nonparametric sign test to obtain a p-value of 0.002 for the 0.06 ppm vs. FA comparison. 

Alternative, more powerful analytic methods using either a Wilcoxon signed-rank test or 

a paired t-test yielded even lower p-values in the EPA analysis. The EPA comparison 

remained significant after a Bonferroni correction for multiple comparisons. The original 

analysis of the data by Adams did not find a significant difference in FEV1 between the 

0.06 and FA exposure conditions. However, that analysis was based on a Scheffe 

correction for multiple comparisons, which is known to have very low power for the type 

of pairwise comparisons conducted by Adams compared to other well-known methods for 

multiple-testing correction (Kirk, 1982).”

“Thus, from my understanding of the statistical analyses that have been conducted, I 

would argue that the analysis by EPA should be preferred to that of Adams for the 

specific comparison of the FEV1 effects of 0.06 ppm exposure relative to FA exposure. Of 

the 30 study subjects in Adams, 24 showed some evidence for an O3-induced decline in 

FEV1, and 2 of the 30 (7%) experienced a decline greater than 10%. Although the 

sample size is relatively small, the consistency of effects across O3 exposure levels, as 

well as the consistency with effects observed by an earlier independent study 

(McDonnell, 2002), indicates that the observed deficits in FEV1 at the 0.060 ppm from 

the Adams study are not spurious. In other words, it is likely that prolonged exposure to 

0.06 ppm O3 causes a general shift in the distribution of FEV1 towards lower values. The 

following plot of the Adams data, derived from Figure 8-2 of Volume I of the “Air 

Quality Criteria for Ozone and Related Photochemical Oxidants, 2006” document, shows 

an approximate normal distribution in the O3-induced changes in FEV1 with exposure to 
284

0.06 ppm.” 

“Although the mean decrement is less than 3% and would not be considered clinically 

important, the shift to the right in this distribution pushes a fraction of subjects into the 

region that becomes clinically interesting (>10%). All of the Adams study subjects were 

healthy volunteers. From a public health standpoint, these results suggest that a large 

number of individuals in the general population (that are otherwise healthy), are likely to 

experience FEV1 deficits greater than 10% with prolonged exposure to 0.06 ppm O3. 

Although most healthy individuals can probably sustain a short-term 10-15% decline in 

FEV1 with little or no noticeable effect, it is not clear how they might be affected in the 

longer term if they experience repeated lung function deficits due to 0.06 ppm or greater 

O3 exposures over multiple days or weeks. Based on several other controlled exposure 

studies, we might expect that O3-induced FEV1 deficits in subjects with an existing 

respiratory condition (e.g. asthma) would be shifted even further to the right compared to 

the above figure. A 10-15% (or greater) pollution-related deficit in FEV1 in an individual 

with an existing respiratory condition is large enough that it could cause a clinically 

observable response.” 

Dr. Rogene Henderson indicated the scientific basis for ozone standard in the range of 0.060 to 

0.070 ppm, based on the controlled human exposure studies, noting the increased sensitivity of 

people with asthma. 

“Human exposure studies provide the most direct evidence of the health effects on 

humans and the studies clearly show that adverse effects occur in some healthy adults 

after exposure for 6.6 hr to 0.060 ppm ozone. This finding has recently been confirmed in 

clinical studies in 59 healthy young adults exposed to 0.060 ppm ozone for 6.6 hours 

(Kim et al., dol:10.1164/rccm.201011-18130C, Lung function and inflammatory 

responses in healthy young adults exposed to 0.060 ppm ozone for 6.6 hours.) Asthmatic 

persons are known to be more sensitive to ozone than are healthy persons. Therefore, to 

provide some margin of safety, the standard must take into consideration these sensitive 

subpopulations.”

Dr. Mort Lippman pointed the large number of people that are impacted by ozone concentrations 

evaluated in the chamber studies: 

“Since the numbers of subjects exposed in the each of the controlled chamber studies at 

each concentration have been small, extrapolation to the much larger general population 

indicates that a very large number of individuals would have substantial responses, even 

though they would constitute only about 10% of the population.”

Dr. Frank Speizer’s comments indicated that susceptible populations might respond more 

severely to ozone exposures tested in the chamber studies. 

“Although the two Adams studies represent the only reported work at levels of exposure 

below 0.080 ppm of ozone, what has been pointed out and what is highly significant is 

that first the studies were done in normals and second that some 7-20% of the subjects 
285

experienced what I would consider very significant lung function decreases (> 10%) and 

or moderate respiratory symptoms. These findings essential preclude, because of the 

ethics of carrying out clinical studies in diseased individuals, from extending these 

studies to what are likely to be an even more sensitive groups. Thus, without having 

specific studies among asthmatics and children at these levels of exposure it is most 

prudent that, in spite of the uncertainty – more later on this issue –that EPA is justified to 

select and exposure level below the 0.080 ppm (and I would say closer to the 0.060 ppm 

level) to ‘protect public health with an adequate margin of safety including the need to 

protect susceptible populations....’”

“Because these results represent a continuum of effects and it is unlikely that there is a 

threshold I would argue that the results are informative and suggest that EPA in carrying 

out its obligation must suggest a standard in the range indicated. I would argue that 

because there is no threshold that the data are consistent with the lower end of the range 

being more protective than the upper end.”

“These small numbers of up to one-fifth of normals of the studied populations having 

changes in lung function or symptoms of this magnitude strongly suggests that the 

susceptible population would respond even greater and could reach clinically significant 

responses that might result in emergency room visits and or hospitalizations.”

Dr. Helen Suh also commented on the adversity of effects in sensitive populations: 

“The scientific evidence from controlled human exposure and epidemiological studies 

and from the exposure and risk assessments supports a primary ozone standard (with a 

margin of safety) between 0.060 to 0.070 ppm. The controlled human exposure studies by 

Adams (2002, 2006) show statistically significant changes in lung function from a 6.6 

hour exposure to 0.060 ppm ozone. While these studies were limited in number, they were 

well designed and results were consistent with those from previous studies, thus lending 

credibility to their findings. Of particular interest is the fact that a small but important 

fraction of the study subjects experienced lung function decrements greater than 10% at 

exposures to 0.060 ppm ozone. These findings suggest that the impacts of ozone 

exposures at these levels may be significant for individuals with pre-existing respiratory 

conditions and must be considered to ensure adequate margin of safety for sensitive 

subpopulations.”

“It is reasonable to consider findings of sub-clinical adverse impacts, such as increased 

inflammation and airway responsiveness, when considering adverse health impacts to 

healthy adults at exposures levels from 0.060 to 0.070 ppm. These findings are certainly 

pertinent to margin of safety considerations.”

“These results provide important evidence that exposures to 0.060 ppm of ozone are 

harmful and are consistent with previous observations of no safe level for ozone 

exposures. Findings from Adams studies (2002, 2006) must be considered, at the least as 

being central to margin of safety determinations.”
286

“For individuals with pre-existing respiratory disease, a 10% decrement in FEV1 is 

significant.”

“Although the sample sizes are small, the variability in the response observed for healthy 

adults in the controlled human studies can inform judgments on the effects of ozone in 

susceptible populations. For example, the 7-20% of healthy adults who were found to 

have large ozone-mediated responses in controlled exposure studies may provide an 

indication of the fraction of individuals in the general population who may also be large 

responders. Ozone-mediated response may comprise an even greater percentage of the 

susceptible population.”

Dr. James Ultman commented on the strengths and weaknesses of the controlled human 

exposure studies. 

“Clinical Studies. Has several strengths including accurate and precise administration of 

exposure gas mixtures and patterns of exposure. The methods of measuring lung function 

and biological responses are also accurate, and precise, and are generally standardized 

between different laboratories. The medical and physiological states of the subjects are 

well-defined. Weaknesses include the use of ozone exposure levels that are usually 0.08 

ppm or above. Only two studies (Adams 2002,2006) were conducted in the range 0.06-

0.07 ppm ozone being considered for the new standard. Also, due to ethical concerns, the 

large majority of all clinical studies are performed on healthy or young subjects or 

subjects with mild respiratory disease. Moreover, only a handful clinical studies 

elucidate the role of copollutants in the exposure gas mixture, and responses are 

observable only when exercise is superimposed on exposure.” 

“The coherence of a substantial amount of data at 0.08 ppm and above also appears to 

be similar between the two labs (table 5-3). This coherence of a substantial amount data 

at 0.08 ppm and above, together with the plausibility of the exposure-response curve that 

passes through the more limited data at 0.06 and 0.04 ppm gives us confidence that 

clinically importance FEV1 responses can occur in moderately exercising subjects at 

0.06 ppm ozone exposure.” 

“Though it only occurs in 7-20% of the subjects, the observation of decrements in FEV1 

>10% at 0.06 ppm ozone exposure is an important indicator of a possible health effect in 

sensitive individuals. The probabilistic exposure-response curve in the staff paper of 

January 2007 (Fig. 5.4) further supports the expectation that, even in a ‘healthy’ 

population, there will be some individuals whose lung function is adversely affected by a 

single 8 hour exposure that includes intermittent moderate exercise.”